**2. Etiopathogenesis**

The life cycle of *T. solium* completes within two hosts (**Figure 1**). Pigs and humans can both act as intermediate hosts for the tapeworm metacestode stage called cysticercus larvae, but humans are the permanent host. During the typical cycle of transmission, the adult *Theridion solium* resides in the human small intestine, where it is affixed to the intestinal wall by its powerful suckers and hooks. The gravid proglottids, which are connected to the worm's distal end, are separated and passed with the faeces, release thousands of viable eggs into the environment. In places with inadequate faeces disposal, pork is fed with human faeces bearing *T. solium* eggs. The eggs shed their outer covers once they are within the pig's digestive tract, releasing oncospheres that go through the intestinal wall and into the circulation before being transported to the tissues, where they develop into cysticercus. Cysticerci are produced in the small intestine, after people consume tainted hog meat, where the action of digestive enzymes leads their scolices to evaginate and adhere to the intestinal wall.

Once the scolex is attached, the proglottids proliferate until they reach maturity 4 months after infection [9]. Humans can act as intermediate hosts for *T. solium* after eating its eggs. Under these circumstances, human cysticercosis can occur. Cysticercosis can be contracted from faeces by people who consume food contaminated with *T. solium* eggs or by those who already have the adult parasite in their intestines. Previous hypotheses that claimed that environmental contamination with *T. solium* eggs was the main cause of human contamination with the parasite have been disproved by recent epidemiological research that shows the clustering of cysticercosis patients near taeniasis patients. Human cysticercosis is considered to be an illness that primarily spreads from person to person, with infected pigs acting as the vehicle for the parasites [10].

**Figure 1.** *Life cycle of Neurocysticercosis (Source: [8]).*

#### *Neurocysticercosis: A Review on Global Neurological Disease DOI: http://dx.doi.org/10.5772/intechopen.110627*

The two main parts of cysticerci are the scolex and the vesicular wall [11]. After entering the central nervous system, cysticerci are in the vesicular (viable) stage, when the parasites have a transparent membrane, clear vesicular fluid, and a characteristically invaginated scolex. Cysticerci may last for years or undergo a degenerative process that causes them to turn into calcifications as a result of the host's immune response. The vesicular fluid becomes murky during the colloidal stage of cysticercal involution, and the scolex shows signs of hyaline degeneration. During the next stage, known as the granular stage, the cyst wall hardens and the scolex changes into mineralised granules. The cysticercus is no longer alive at this moment. Finally, the parasite remains are visible as a mineralised nodule [12]. The tissue around vesicular cysticerci does not experience considerable inflammation. In contrast, the parasite is typically wrapped in a collagen capsule, with a mononuclear inflammatory response surrounding colloidal cysticerci.

The surrounding brain parenchyma exhibits astrocyte gliosis, microglial proliferation, oedema, neuronal degenerative changes, and lymphocyte perivascular cuffing. When the parasites reach the granular and calcified phases, the oedema disappears; however, the astrocytic changes around the lesions may worsen. Epithelioid cells also begin to grow and assemble into multinucleated big cells at this time. Meningeal cysticerci often cause a strong inflammatory response in the subarachnoid space and aberrant thickening of the leptomeninges. This exudate contains collagen fibres, lymphocytes, multinucleated giant cells, eosinophils, and hyalinized parasite membranes [13]. Widespread inflammation may cause damage to cranial nerves, the optic chiasm, and small penetrating arteries that arise from the circle of Willis.

The latter might result in a blockage of the vessel's lumen, which would cause a cerebral infarction to form [14]. Ventricular cysticerci may potentially trigger an inflammatory response if they are linked to the choroid plexus or the ventricular wall.

While certain cysticerci antigens aid in the evasion of the immune system's defences against cysticerci, other cysticerci antigens, including (especially antigen B),

#### **Figure 2.**

*Transmission of Neurocysticercosis. Source: https://journals.plos.org/plosntds/article/figures?id=10.1371/journal. pntd.0 008005*

cause the production of particular antibodies that constitute the cornerstone of the cysticercosis immunological diagnosis [15]. Furthermore, it has been postulated that increased subpopulations of CD8 T-lymphocytes, poor lymphocyte proliferation, and aberrant cytokine concentrations in neurocysticercosis patients lead to cellular immunological dysfunction. According to the studies, immunodeficiency conditions and the growth of gliomas are associated with neurocysticercosis [16].

According to a notion, the immune system may find it challenging to detect malignancy in these circumstances due to the high levels of glial proliferation around the parasites and the inhibition of cellular immune responses, resulting in the malignant transformation of astrocytes (**Figure 2**) [17].
