Neurocysticercosis (NCC) is the most important parasitic infection of the human central nervous system and a leading cause of adult-onset seizures and epilepsy in many low- and middle-income countries where the parasite is endemic (Garcia et al., 2014; Gripper and Welburn, 2017). It results from CNS infection with the larval stage of Taenia solium, a zoonosis tightly linked to poverty, free-roaming pigs, poor sanitation, and inadequate meat inspection (Garcia et al., 2014; Mwape et al., 2013). Human infection follows ingestion of T. solium eggs, with larvae encysting in brain parenchyma, ventricles, subarachnoid spaces, or ocular structures. Over the past 2 decades, however, the field has undergone a fundamental transition. NCC is now recognized as a heterogeneous neuroinflammatory disease encompassing multiple well-defined clinical syndromes, shaped by parasite location, developmental stage, parasite burden, and host immune response. The clinical framework has evolved from a seizure-centric model to a syndrome-based approach that includes extraparenchymal disease, neuropsychiatric syndromes, movement disorders, hydrocephalus, cognitive impairment, and visual loss (Mahale et al., 2015; Singh et al., 2024). The diagnostic strategies have expanded beyond conventional neuroimaging to include refined serological assays, point-of-care antigen tests, and molecular tools, enabling earlier and more precise case identification. At the same time, treatment paradigms have shifted from uniform antiparasitic therapy to individualized regimens that integrate antiparasitic drugs, staged corticosteroid strategies, and neurosurgical or endoscopic interventions when indicated.

NCC is highly endemic across Latin America, sub-Saharan Africa, and parts of South and Southeast Asia, where human tapeworm carriers, environmental egg contamination, and pig exposure coexist (Garcia et al., 2014; Mahale et al., 2015). Community-based studies in endemic areas suggest that T. solium cysticercosis may affect 10%–20% of the population serologically, with a substantial fraction of active or calcified brain lesions detectable on CT (Gripper and Welburn, 2017). In some rural regions of Latin America and India, NCC is estimated to account for up to one-third of cases of adult-onset epilepsy (Garcia et al., 2014; Mahale et al., 2015). Beyond traditional endemic zones, NCC has become an important globalized infection. Increased migration, travel, and globalized food chains have led to rising numbers of cases in North America and Europe, often in migrants or their close contacts (Gripper and Welburn, 2017). Autochthonous transmission has been documented in several high-income countries when a tapeworm carrier contaminates food, as illustrated by a school outbreak in Belgium (Vanden Driessche et al., 2024). These events show that NCC is possible wherever basic sanitation and carrier detection fail, regardless of national income level.

From a neurological standpoint, NCC is now recognized as a major cause of epilepsy burden. A large cohort analysis confirmed a strong association between calcified NCC and mesial temporal lobe epilepsy with hippocampal sclerosis, emphasizing its role in chronic epileptogenesis (Secchi et al., 2021). In endemic areas, NCC also contributes to headache disorders, cognitive impairment, and stroke, particularly in subarachnoid and intraventricular forms (Mahale et al., 2015; Vasquez-Baiocchi et al., 2025).

Humans acquire taeniasis by ingesting cysticerci in undercooked pork, becoming definitive hosts harbouring adult tapeworms in the small intestine, which shed eggs and proglottids into the environment. Pigs, the normal intermediate host, ingest eggs and develop muscular cysticerci, completing the pig–human cycle. Neurocysticercosis arises when humans instead ingest T. solium eggs (contaminated food, water, or via autoinfection), acting as aberrant intermediate hosts. In the small intestine, the scolex evaginates, attaches to the mucosa, and matures into an adult tapeworm that sheds gravid proglottids and eggs in feces, contaminating soil, water, and food. Pigs ingest these eggs, the oncospheres hatch, penetrate the gut wall, and travel via the bloodstream to muscle, where they encyst as cysticerci (“measly pork”), completing the classical pig–human cycle. NCC emerges when humans instead ingest eggs (contaminated food/water or autoinfection in a tapeworm carrier), becoming aberrant intermediate hosts (Figure 1). Oncospheres hatch in the human intestine, penetrate the mucosa, and disseminate hematogenously to the brain, spinal cord, eye, and other tissues, producing systemic cysticercosis and, when the CNS is involved, resulting neurocysticercosis (Garcia et al., 2014; Gripper and Welburn, 2017).

The clinical and radiologic course is largely determined by the stage of the cyst and the intensity of the host immune response. Within the CNS, larvae encyst and develop into cysticerci in different compartments: brain parenchyma, subarachnoid spaces, ventricular system, spinal canal, and ocular structures. In parenchymal NCC, cysts evolve through four main stages: vesicular, colloidal, granular–nodular and calcified (Table 1).

In the vesicular (viable) stage, cysticerci are thin-walled, fluid-filled vesicles with a visible scolex, surrounded by minimal inflammation. The parasite actively down-modulates local immunity, favouring regulatory and anti-inflammatory pathways and limiting oedema and gliosis (Prodjinotho et al., 2020). Many patients remain asymptomatic, but seizures or headaches can occur when lesions are numerous or cortically located. On imaging, these appear as CSF like cysts with the classic “hole-with-dot” sign. As the parasite begins to degenerate, the lesion enters the colloidal stage, which is the most pathogenic phase. Cyst wall breakdown and antigen leakage trigger a vigorous inflammatory reaction with activation of microglia, macrophages, and T cells, and production of pro-inflammatory cytokines such as TNF-α, IL-1β, and IL-6 (Miltenberger et al., 2025). The blood–brain barrier becomes disrupted, leading to marked perilesional oedema and mass effect. Clinically, this corresponds to acute symptomatic seizures, severe headache, focal deficits, and signs of raised intracranial pressure. CT and MRI typically show ring-enhancing lesions with extensive oedema (Garcia et al., 2014).

With time, inflammation becomes organised and the lesion transitions to the granular–nodular stage. The cyst collapses and is replaced by a smaller fibrotic granuloma; oedema recedes and enhancement diminishes. Symptoms often improve, but seizures may persist as networks reorganise around the lesional scar (Secchi et al., 2021). Ultimately, the lesion becomes a calcified nodule, representing an “inactive” but often epileptogenic stage.

In extraparenchymal NCC, disease is driven by inflammation and obstruction of cerebrospinal fluid spaces. Subarachnoid (racemose) NCC involves large, multiloculated cysts in the basal cisterns and fissures, causing chronic eosinophilic meningitis, arachnoiditis, and fibrosis, which result in hydrocephalus, cranial neuropathies, and inflammatory vasculitis with increased stroke risk. Intraventricular NCC causes mechanical obstruction of CSF flow and ependymitis, resulting in intermittent or acute obstructive hydrocephalus and potential sudden deterioration (Xu et al., 2025).

The same principles apply in ocular and spinal disease, where cysts in tight, functionally critical spaces provoke disproportionate damage through local inflammation and mass effect. Ocular cysts can cause vitreitis and retinal detachment; killing an intraocular cyst without prior surgical removal can trigger catastrophic inflammation and vision loss (Garg et al., 2025a). Spinal cysts may cause arachnoiditis, cord compression, and progressive myelopathy. Systematic reviews show NCC as a reversible cause of parkinsonism, chorea, dystonia, and other hyperkinetic syndromes, as well as significant vision loss from ocular and neuro-ophthalmic involvement (Garg et al., 2025a; Garg et al., 2025b).

Overall, NCC pathophysiology reflects a dynamic interplay between parasite stage and host immunity, evolving from immune evasion and silent infection to intense inflammatory injury and, finally, to a scarred but persistently epileptogenic CNS (Cangalaya et al., 2017; Torib et al., 2024). Frontal lobe NCC presenting predominantly with schizoaffective-like symptoms in an adolescent immigrant illustrates how lesions can masquerade as primary psychiatric disease, with improvement following antiparasitic therapy and antipsychotics (Annor et al., 2025). Racemose and intraventricular forms often present with hydrocephalus, cranial neuropathies, and complex CSF-flow disturbances, demanding combined neurosurgical–medical care (Mahale et al., 2015; Xu et al., 2025). These findings support a shift from viewing NCC purely as a seizure disorder toward a broader “neurocysticercosis syndrome” encompassing epilepsy, neuropsychiatric, ocular, motor, and cognitive domains.

Although NCC predominantly involves the central nervous system, T. solium larvae may also affect subcutaneous tissue and skeletal muscle. Subcutaneous cysticercosis typically presents as painless nodules, while muscular involvement may be asymptomatic or cause myalgia or pseudohypertrophy during cyst degeneration (Del Brutto, 2012). Imaging and serology aid diagnosis, and recognition of these extracranial forms supports evaluation for concurrent NCC and guides management decisions.

NCC is undergoing a fundamental transition from a seizure-focused parasitic infection to a spectrum of well-characterized neuroinflammatory syndromes encompassing epilepsy, cognitive impairment, psychiatric manifestations, movement disorders, hydrocephalus, and visual loss. Advances in diagnostics, deeper understanding of host–parasite immunology and evolving pharmacologic and surgical strategies have transformed clinical care, while also revealing persistent evidence and implementation gaps. By adopting a phenotype-driven and context-sensitive approach, clinicians can improve diagnostic precision, tailor therapy to disease compartment and inflammatory risk, and reduce preventable complications. Embracing this transition perspective in both endemic and non-endemic settings offers a pathway toward improved patient outcomes and reduced global neurological disability from NCC.