*4.5.2 Mechanisms of hydrocephalus*

Hydrocephalus in NCC can result from various mechanisms [38–42];

a.**Obstructive hydrocephalus:** One of the pivotal determinants of NCC-related neuropathologies is the size of the cysticerci within the central nervous system. Large cysts, when present, exert localized pressure on adjacent neural structures, leading to a spectrum of neurological deficits [20, 22, 24, 26]. This pressure effect can disrupt normal neuronal function, resulting in focal symptoms such

as seizures, sensory deficits, and motor impairments. Moreover, the compression of blood vessels by these cysts may compromise cerebral perfusion, precipitating ischemic events and further exacerbating the clinical picture [20, 22, 24, 26].

a.Aggregation of multiple cysts:

In certain instances, NCC takes on a more complex manifestation, characterized by the aggregation of multiple cysts into a single large bundle or cluster. This phenomenon intensifies the pressure effects within the confined intracranial space. The aggregative growth of cysticerci not only exacerbates focal neurological deficits but can also lead to increased intracranial pressure (ICP) [24, 43–45]. Elevated ICP is a grave concern, potentially giving rise to severe headaches, papilledema, and, in extreme cases, herniation syndromes. Timely intervention is imperative to alleviate these critical pressure-related consequences [24, 43, 44].

Cysts located in the ventricular system or causing obstruction to the flow of CSF can lead to obstructive hydrocephalus. The cysts physically block CSF flow, resulting in fluid accumulation and increased intracranial pressure. The obstruction can occur at the foramen of Monro, cerebral aqueduct, or fourth ventricle, depending on the location of the cysts [38–42].

b.**Non-obstructive hydrocephalus:** Inflammation and scarring induced by the infection can disrupt CSF's normal absorption or impair the ventricular system's flow dynamics. This can result in impaired CSF circulation and non-obstructive hydrocephalus [38–42].

Hydrocephalus associated with NCC can present with various symptoms depending on the severity and rapidity of CSF accumulation. Common clinical manifestations include headache, nausea, vomiting, papilledema (swelling of the optic disc), visual disturbances, gait disturbances, cognitive changes, and altered consciousness or coma in severe cases.

#### **4.6 Obstruction of cerebrospinal fluid pathways**

Another intriguing facet of NCC-related neuropathologies pertains to the obstruction of CSF pathways by cysticercal lesions. When cysts infiltrate the CSF circulation, they may impede the flow of this vital fluid, resulting in conditions such as hydrocephalus. The accumulation of CSF within the ventricular system can cause ventricular dilation and elevate ICP. Recognizing and addressing these obstructive patterns is crucial to preventing secondary complications associated with increased intracranial pressure [43, 45–47].

Neurocysticercosis exhibits an intricate interplay between its insidious onset and the subsequent emergence of neuropathological manifestations. While the initial stages of the disease may remain asymptomatic, the potential for neurological deficits becomes increasingly pronounced as the cysticerci grow and interact with their neural surroundings. Pressure effects arising from large cysts, the aggregation of multiple cysts, and the obstruction of cerebrospinal fluid pathways constitute critical determinants in the clinical trajectory of NCC. Early recognition, accurate diagnosis, and prompt management are imperative to mitigate the neurological sequelae associated with this parasitic infection.
