This case illustrates the image findings of a patient with neurocysticercosis.
Neurocysticercosis is caused by the infection of the central nervous system (CNS) with encysted larvae of Taenia solium 1. The lifecycle of Taenia solium 1,2 comprises of human ingestion of swine meat infected with lava (cysticercus/ cysticerci). Within the human host, the cysticerci attach to the intestinal wall, where they gradually mature into tapeworm. The female tapeworm releases fertile eggs, containing infective embryos, some of which are released from the egg within the intestines, actively cross the intestinal mucosa into the bloodstream, thereby traveling to peripheral tissues including the central nervous system 3.
The remaining embryos are passed into the environment through human feces where a combination of poor sanitation and open defecation leads to soil contamination with these fertile eggs. Pigs after that can ingest the infective eggs in human stools whilst grazing on the contaminated soil. The eggs hatch into larvae in the pig’s intestine that pass through the mucosa and reach various tissues, where they mature into cysticerci. The life cycle is once again thereby propagated upon human consumption of this swine meat.
Taenia solium is endemic in most developing countries, particularly Latin America, Southeast Asia, and wide parts of sub-Saharan Africa 1. The clinical manifestations of neurocysticercosis include seizures, headache, cognitive decline, intracranial hypertension and focal neurological deficits; although no pathognomic clinical picture exists 4. Taken together with the clinical picture, diagnosis is based on neuroimaging and confirmed by serology.
Cysticerci in the CNS may be located in the brain parenchyma, subarachnoid space, ventricles, or spinal cord 4.
Parenchymal neurocysticercosis can be classified into four discrete disease stages: vesicular, colloidal vesicular, granular nodular and nodular calcified 2. Imaging findings in each stage reflect underlying changes in the disease process 4-6:
- In the vesicular stage, the cystericus contain clear fluid. These are readily discernible on CT and MRI, measuring at 5-20mm. CT demonstrates non-enhancing cyst wall contained a scolex with CSF density cystic fluid. T1-weighted MR imaging demonstrates a low-signal-intensity cystic cavity containing a nodule that is isointense/hyperintense about white matter. On T2-weighted images, the scolex is also isointense/hyperintense and can be obscured by high-signal intensity cystic fluid. Cysts commonly occur at the gray-white matter junction, basal ganglia, cerebellum, and brainstem.
- The colloid vesicular stage is characterized by hyaline degeneration of the cysticercus. Fluid within the cyst becomes proteinaceous, opaque and gelatinous, eliciting a strong immune response as it leaking into surrounding tissue. CT demonstrates ring-enhancing cystic lesions containing hyperdense fluid, and surrounding vasogenic edema. On MRI, T1-weighted images show a cystic cavity hyperintense to CSF, and on T2, hyperintense cyst surrounded by hyperintense parenchymal edema.
- In the granular nodular stage, the cyst retracts and forms a granulomatous nodule. CT demonstrates an enhancing nodule with surrounding vasogenic edema. MR shows enhancing ring or nodule with or without surrounding edema.
- The nodular calcified stage is characterized calcification of the granulomatous nodule. CT demonstrates calcified lesions within the brain parenchyma, which appear isointense on all MR imaging sequences.
Cisternal cysticercosis is characterized by disease involvement of the subarachnoid spaces and adjacent meninges 4 and may manifest as obstructive hydrocephalus on CT and MRI 5. The latter is also true of intraventricular cysticercosis. Spinal cysticercosis is uncommon, and if present, can appear as a ring-enhancing lesion expanding the spinal cord on MRI 4.
Treatment of neurocysticercosis involves 4-6:
- control of seizures: antiepileptic treatment
- anti-parasitic medication (cysticidal therapy)
Case courtesy of Associate Professor Pramit Phal