Neurocysticercosis (NCC) is caused by CNS infection with the pork tapeworm Taenia solium 2.
Demographics and clinical presentation
The disease is endemic in Central and South America, Asia and Africa. There is a variable time interval between point of infection and the onset of symptoms (ranging from 1-30 years). Clinical presentation includes 1:
- seizures: most common cause of seizures in young adults in endemic areas 2
- altered mental status
- neurological deficits
CSF serology may be helpful with the initial diagnosis especially in cases of intraventricular/subarachnoid infection 2.
Infection which leads to extra-intestinal disease (including neurocysticercosis) usually occurs as a result of eating food or drinking water contaminated by human feces containing T. solium eggs. This is distinct from the 'normal' life cycle in which the undercooked pork is eaten and the larval cysts contained within mature into adult intestinal tape worm 3.
Extra-intestinal infection undergoes specific clinical and imaging changes at it progresses through four stages of infection 1.
There are four main stages (also known as Escobar's pathological stages):
- Vesicular: viable parasite with intact membrane and therefore no host reaction.
- Colloidal vesicular: parasite dies within 4-5 years 1 untreated, or earlier with treatment and the cyst fluid becomes turbid. As the membrane becomes leaky oedema surrounds the cyst. This is the most symptomatic stage.
- Granular nodular: oedema decreases as the cyst retracts further; enhancement persists.
- Nodular calcified: end-stage quiescent calcified cyst remnant; no oedema.
Infection can be both intra and extra axial. Commonest location is the subarachnoid space over the cerebral hemispheres. Other locations in order of decreasing frequency are:
- subarachnoid space over the cerebral hemispheres
- may be large
- basal cisterns
- may be "grape like" (racemose): most lack an indentifiable scolex
- usually solitary cysts
- 4th ventricle most frequent
Typically the parenchymal cysts are small (1cm) whereas the subarachnoid ones can be much bigger (up to 9cm): differential therefore being arachnoid cyst.
It is the most common cause of epilepsy in endemic areas (South-east Asia, South America) with progression through the 4 stages taking anywhere between 1 to 9 years.
Imaging findings depend on location and stage of infection.
When in the subarachnoid space/intraventricular, the the cysts typically do not have a visible scolex. In the basal cisterns they can be grape-like (racemose). The cysts are typically 1-2 cm in diameter 2. Usually the cysts are similar in signal intensity to CSF, although occasionally cyst fluid may somewhat differ 2.
Parenchymal cysts usually involve the grey white matter junction 2.
- cyst with dot sign
- CSF density/intensity
- hyperintense scolex on T1 can sometimes be seen
- no enhancement is typical, although very faint enhancement of the wall and enhancement of the scolex may be seen
- cyst fluid becomes turbid
- CT: hyperdense to CSF
- MRI T1: hyperintense to CSF 2
- surrounding oedema
- cyst and the wall becomes thickened and brightly enhances
- scolex can often still be seen as an eccentric focus of enhancement
- oedema decreases
- cyst retracts
- enhancement persists but is less marked 1
- endstage quiescent calcified cyst remnant
- no oedema
- no enhancement on CT
- signal drop out on T2 and T2* sequences
- some intrinsic high T1 signal may be present
- long term enhancement may be evident on MRI, and may predict ongoing seizures 1
General imaging differential considerations include:
- 1. Sheth TN, Pillon L, Keystone J et-al. Persistent MR contrast enhancement of calcified neurocysticercosis lesions. AJNR Am J Neuroradiol. 1998;19 (1): 79-82. AJNR Am J Neuroradiol (abstract) - Pubmed citation
- 2. Teitelbaum GP, Otto RJ, Lin M et-al. MR imaging of neurocysticercosis. AJR Am J Roentgenol. 1989;153 (4): 857-66. AJR Am J Roentgenol (abstract) - Pubmed citation
- 3. Kumar V, Abbas AK, Fausto N et-al. Robbins and Cotran pathologic basis of disease. W B Saunders Co. (2005) ISBN:0721601871. Read it at Google Books - Find it at Amazon
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