- Clinical findings relate to the number, location, and size of cysts: NCC should be suspected in patients coming from endemic areas with sudden-onset seizures, headache, vomiting, or focal motor deficits when there is no other evidence of an underlying neurological disorder. Infested individuals may be completely asymptomatic for a long time, especially in the early stages of dissemination (1,14,25,32).
- Heterogeneous presentation: Mental disorders, focal neurologic deficits, and signs and symptoms of space-occupying intracranial lesions may also be present. Death can occur suddenly. Duration of symptoms on admission ranges from hours to several years (1,5).
Axial T2-weighted MRI of an isolated cysticercus in the colloidal stage. The MRI appearance somewhat simulated a brain tumor (A). The surgical specimen is seen with the capsule open (B)
- Seizures: Long-standing or even recent-onset seizures are by far the most common manifestation of NCC (4,9,10). Approximately 30% of people with cysticercosis have epilepsy in developing countries and NCC accounts for more than 80% of the cases of epilepsy where it is edemic (3). It accounts for 50% of the cases of late-onset epilepsy in low-income countries (22,38,39). Degenerating parenchymal cysts very often lead to seizures. In Indian children, the most common presentation of NCC is the SCG (1,2,5,7,8,23)
- Focal neurological deficits – multiple etiologies: This can result from parenchymal brain cysts, from pericystic edema, or mass effects of large subarachnoid cysticerci. The occlusion of small cerebral arteries may cause strokes. Compression of any cranial nerves can cause specific deficit. Spinal cord cysts may lead to motor or sensorial deficits and radicular pain (40,41).
- Intracranial hypertension – causes: Elevate ICP can be caused directly by obstructive or communicating hydrocephalu[RA1] s, large subarachnoid cysts, or a severe inflammatory response that characteristically affects children and women in the first three decades of life causing encephalitis and diffuse brain edema. The encephalitis often occurs in children and young women who have not had contact with the parasite until they are infected with a substantial load of eggs, causing an aggressive reaction by the immune system against the parasites (42,43)
CAT scan and MRI of ventricular enlargement due Cysticercus. Cysticercus inside the ventricles may narrow or block CSF pathways mechanically or because of inflammatory changes. In this case, blockage of the fourth ventricle is seen in C (arrow).
- Meningeal signs: Nausea, vomiting, headache may be present. (5,12,25).
- Altered mental state and focal neurological deficits: Neurocognitive deficits, mental disorders, focal neurologic deficits, and signs and symptoms of space-occupying intracranial lesions may be present (26,30,34).
- Cysticercal encephalitis: Epilepsy, brain edema, and intracranial hypertension are associated with cystercal encephalitis. This form of NCC may be fatal (5,8,26).
- Strokes: Ischemic or hemorrhagic strokes may result from NCC. They are usually due to occlusive arteritis of small perforating vessels, resulting in lacunar infarcts. Large-vessel strokes and hemorrhage occur but are less common (30,31).
- Sudden death: This is rare, and in these cases, NCC is an autopsy finding (1,5).
Time for evolution
- Long asymptomatic period: Infested individuals may be completely asymptomatic, especially in early stages of dissemination. The asymptomatic state can last for a long time. The duration of symptoms at admission ranges from hours to several years (1,25).