A 34-year-old rural male patient with no relevant past medical history, presents to the emergency department with new onset of seizure, headache and confusion.
Non-enhanced CT images in Fig 1a and b show a hypodense, well-defined, extra-axial cystic lesion with mass effect that crosses the mid-line.
MRI sequences in Fig 2a demonstrate similar signal intensity within the the lobulated cysts compared to cerebrospinal fluid (CSF) and no evidence of surrounding vasogenic oedema. Note that the signal intensity of the anterior cyst presents mild hypointensity on FLAIR images compared to CSF due to its proteinaceous material content. Cysts have a lobulated appearance resembling a cluster of grapes (racemose). There is no evidence of restricted diffusion.
Fig 2b and c reveal a round hypointense structure within the cyst representing the scolex (blue arrow). Figures 2d and e show peripheral enhancement of the thin walls of the cyst (yellow arrow) with no internal enhancement.
Neurocysticercosis is considered the most common parasitic disease in the central nervous system and the most common cause of acquired epilepsy[1, 2].
Consumption of undercooked pork meat infected with cysticercus begins the life-cycle. In the human digestive tract the scolex (parasites head) emerges from the cyst and forms proglottids that self-fertilise and originate new eggs. In the next stage, ingestion of food/beverages contaminated with Taenia solium eggs form oncospheres; afterwards they cross the intestinal wall into the bloodstream and invades different organs with a preference for where they can go unnoticed by the immune system, like the eyes and central nervous system [2, 3].
Approximately 75 million people in Latin America are at risk for neurocysticercosis of whom only a minority with incidental calcified granulomas found in brain parenchyma develop symptoms . Three mechanisms by which cysticerosis cause symptoms include: 1) Presence of the parasite itself, leading to mass effect and obstruction, 2) Inflammatory response and 3) Residual scarring (fibrosis, granulomas and calcifications) . Seizures are the most common clinical expression followed by headache, focal neurological deficits and increased intracranial pressure [2, 3].
Neurocysticercosis can be divided into intraparenchymal(~80%) or extraparenchymal (~20%). The latter, depending on its location, may be intraventricular and/or subarachnoid where its variant racemose neurocysticercosis may occur .
Radiologic findings divide neurocysticercosis in five stages: 1)Non-cystic; parasitic invasion without oedema, asymptomatic phase, 2) Vesicular; cysts with scolex, 3) Colloidal-vesicular; parasite dies, marked oedema and no scolex present, 4) Granular-nodular; cyst absorb and start to retract and 5) Calcified-granular; calcified granulomas are present [2, 5].
Diagnosis of racemose neurocysticercosis is based on neuro imaging, serum (antibodies) and laboratory (CSF) evaluation. History of travel to disease-endemic areas may aid in the diagnosis . CT imaging has high sensitivity and specificity in the diagnosis of intraparenchymal neurocysticercosis, but it is low for extraparenchymal forms .
MRI with gadolinium is the modality of choice for diagnosis. Lesions appear with high signal intensity on T2WI, similar to CSF, and depict delineation of the thin cyst wall. Obstructive or communicating hydrocephalus may be present [3, 6]. Leptomeningeal enhancement secondary to arachnoiditis may appear . Little oedema or none is noted. Cyst can measure 5–20mm and a cluster of cysts resembling a “cluster of grapes” appearance may be present [1, 5].
Medical and surgical treatment are the mainstay management. Purpose of treatment involves management of symptoms and associated disease sequelae. Most common anti-parasitic drugs are albendazole or praziquantel. Surgical intervention for resection (open or endoscopic) dependent on cyst location can help, while in some cases medical treatment alone is sufficient .
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