**1. Introduction**

Taeniasis and cysticercosis (T/C) are zoonotic infections caused by tapeworms of the genus *Taenia*. Humans are definitive hosts for three *Taenia* species that can cause human taeniasis: *Theridion solium*, *Theridion saginata*, and *Torenia asiatica* [1]. Cysticercosis refers to the tissue infection of the intermediate host: bovines for *T. saginata* and pigs for *T. solium* and *T. asiatica*—the first one is endemic to many developing regions, while the latter is restricted to some Asian countries [2]. Humans can get infected by ingesting raw or undercooked meat contaminated with cysticerci (larval cysts). However, humans can get infected with *T. solium* by consuming food or water contaminated with parasite eggs and act as dead-end intermediate hosts, developing cysticercosis. This infection often leads to neurocysticercosis (NCC), a major cause of epilepsy associated with considerable morbidity and mortality [3].

Neurocysticercosis is currently the most prevalent helminthic infection of the central nervous system (CNS). Although its prevalence is unknown, millions of people are likely infected with this parasite, and many eventually develop clinical symptoms. Most nations in Latin America, sub-Saharan Africa, and parts of Asia have endemic NCC. However, it is not typical in Northern Europe, the US, Canada, Australia, Japan, or New Zealand—except among immigrant communities [4].

*T. solium* and *T. saginata* are flat, segmented, and hermaphrodite parasites measuring 2–10 m. Adult parasites are located in the small intestine. They comprise a head or scolex—with a diameter of ~1 mm bearing four muscular suckers for fixation and some form of locomotion. Unlike *T. saginata*, *T. solium* has an armed rostellum bearing 22–36 hooks ordered in two rows. A thin neck measuring ~5–10 mm constitutes the portion with the most biokinetic activity; the entire body—or strobila—is formed from this part [5]. The adult *T. asiatica* worm measures 3.41 m in length and 9.5 mm in width and comprises 712 segments. The scolex of adult or larva *T. asiatica* has four suckers of 0.24–0.29 mm in diameter and a cuspidal rostellum with a maximal width of up to 0.81 mm. The maximum width of the *T. asiatica* scolex is 1.5 times smaller than that of *T. saginata* [6]. The strobila of *Taenia* species comprises 800–4000 proglottids—or segments—divided into immature, mature, and gravid segments. Immature segments are wider transversely than longitudinally, whereas mature segments are square, with primary sexual organs fully developed. Finally, gravid segments are rectangular, with the longest axis running lengthwise; most primary genital organs are atrophied, while the uterus is almost entirely branched and filled with oncospheres.

Oncospheres, or spherical eggs, are found in the uterus and range from 29 to 77 μm for *T. solium*, 39 to 50 μm in *T. saginata*, and 33.8 to 40 μm in *T. saginata*. The eggs of *Taenia* species cannot be distinguished by conventional light microscopy [7]. A cysticercus is an ovoid vesicle with a translucent membrane and a 5–15 mm diameter. It is filled with a colorless liquid and has an invaginated scolex. The larval stage is called *Cysticercus* spp., more appropriately called a "metacestode" of *Taenia* spp. The term "cysticercus racemosus" is frequently used to describe a wild-growing *T. solium* cysticercus in humans. This metacestode has a degenerative form and is found in the meninges and ventricular system of the brain. Cysticerci can persist in the brain for many years before patients experience symptoms; in some instances, they may never. Pleomorphic symptoms and signs are frequently brought on by the degradation of cysticerci and the accompanying host immunological response. Epileptic seizures, headaches, focal neurological impairments, and indicators of elevated intracranial pressure are the most typical symptoms. Neurological manifestations depend on the number—single or multiple—size, location (e.g., intraparenchymal or extraparenchymal), stage of the cysticerci—viable or calcified—and the host's immune response [8].

Researchers have been trying to develop diagnostic techniques to detect the presence of parasites within bodily tissues since the early 20th century. Counting white blood cells, specifically eosinophils, was an initial nonspecific test that raised the possibility of infections [9]. Serological tests for circulating antibodies (Abs) were created very quickly. Although unable to distinguish between active and dormant infections, antibody detection proved to be a better attempt at diagnosis, with greater predictive values than the earlier eosinophil counting [10]. The enzyme-linked immunosorbent test (ELISA), introduced in 1971, quickly gained popularity as the preferred method for detecting antibodies; it was the most sensitive method available at the time to process multiple samples simultaneously [11]. Computed Tomography (CT) and Magnetic Resonance Imaging (MRI), developed in 1977 and 1986, respectively, significantly improved the classification of NCC features [12]. These scans made it easier for clinicians to make definitive diagnoses based on the size, type, stage, and location of cysticerci in the patient's CNS. Neuroimaging is still the reference standard today.
