Chapter 72 Neurophysiological aspects of cerebral cysticercosis

Abstract

Taeniasis/cysticercosis is a parasitic disease that has become a worldwide health issue because of the increasing immigration from frequent travel to endemic regions. These parasitic diseases are related to poverty and deficient sanitary infrastructure. Neurocysticercosis (NC) is associated with seizures, headache, and focal neurological deficits and may lead to long-term neurologic sequelae, such as epilepsy, hydrocephalus, and dementia. Seizures are the most common symptom in patients with NC; however, there are inconsistencies in the link between epilepsy and NC. This chapter discusses the available information, regarding electroencephalographic abnormalities, in patients with NC. Humans are the only known host harboring the adult cestode parasite Taenia solium in the intestine. Infection is acquired by ingesting undercooked pork infected with Taenia larvae (cysticerci). The chapter details the life cycle of cestode parasite. Human cysticercosis is acquired from the “accidental” ingestion of ova excreted by human tapeworm carriers in their feces. In humans the commonest routes of infection are ingestion of T. solium eggs, from contaminated food and fecal-oral auto infestation, in patients harboring the adult parasite in their intestines. Cysts can develop in any human tissue, but they have a predilection for the central nervous system (CNS), skeletal muscle, subcutaneous tissue, and the eye. The parasites arrive at the CNS via blood vessels and tend to locate in the irrigated gray matter. Immunoserologic assays detect antibodies against T solium or cysticercus. These assays are useful for the identification of individuals who have had systemic contact with the parasite at some time. The “gold standard” for diagnosing NC is pathologic confirmation through biopsy or autopsy. Seizures are the most common symptom of NC. The chapter notes the EEG abnormalities in patients with neurocysticercosis. Studies suggested that perilesional gliosis might be insufficient to cause scalp EEG abnormality in the inactive form of NC.