Neurocysticercosis is caused by the CNS infection with the pork tapeworm Taenia solium, which is endemic in most low-income countries where pigs are raised. This form of cysticercosis is a relevant cause of seizures in endemic areas.
The disease is endemic in Central and South America, Asia and Africa. The perpetuation of this parasitic disease is related to poor sanitation and hygiene.
There is no gender or race predilection and most symptomatic patients are aged 15-40 years 4.
There is a variable time interval between the point of infection and the onset of symptoms (ranging from 1-30 years).
Clinical presentation includes 1:
- seizures: most common symptom and the most common cause of seizures in young adults in endemic areas 2
- altered mental status
- neurological deficits
- Bruns syndrome: caused by cysticerci cysts of the third and fourth ventricle 4
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 tapeworm 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 edema surrounds the cyst. This is the most symptomatic stage.
- granular nodular: edema decreases as the cyst retract further; enhancement persists.
- nodular calcified: end-stage quiescent calcified cyst remnant; no edema.
Infection can be both intra- and extra-axial. Commonest locations are 3-5:
- subarachnoid space over the cerebral hemispheres: can be very large
- parenchyma: most common location, frequently seen near the grey matter-white matter junction 4
- basal cisterns
- maybe "grape-like" (racemose): most lack an identifiable scolex
- usually solitary cyst
- 4th ventricle: most frequent location
- spinal forms: associated with concomitant intracranial involvement 4
Typically the parenchymal cysts are small (1 cm) whereas the subarachnoid cysts can be much bigger (up to 9 cm): differential, therefore, being an arachnoid cyst.
Imaging findings depend on the location and stage of infection.
When in the subarachnoid space/interventricular, 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.
Each stage has fairly distinctive imaging features although there is no sharp demarcation between later stages.
- cyst with dot sign
- CSF density/intensity
- eccentric 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 6
- no surrounding vasogenic edema
- cyst fluid becomes macroscopically turbid reflected in altered imaging appearance:
- CT: hyperattenuating to CSF
- MRI T1: hyperintense to CSF 2
- surrounding edema
- cyst and the wall become thickened and brightly enhances
- scolex is seen early in the colloidal phase but gradually shrinks down and is harder to identify 6
- edema decreases
- cyst retracts eventually becoming a small enhancing nodule 6
- enhancement persists but is less marked 1
- end-stage quiescent calcified nodule
- no edema
- 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
Treatment and prognosis
The treatment options available to patients with neurocysticercosis include symptomatic therapy (e.g. anti-epileptics) and anthelmintic therapy (e.g. albendazole and praziquantel, the two antiparasitics most commonly used 4), usually accompanied by corticosteroids. Surgery (e.g. VP shunt placement or decompression) is only rarely indicated.
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
- 4. Kimura-Hayama ET, Higuera JA, Corona-Cedillo R et-al. Neurocysticercosis: radiologic-pathologic correlation. Radiographics. 2010;30 (6): 1705-19. doi:10.1148/rg.306105522 - Pubmed citation
- 5. Nash TE, Garcia HH. Diagnosis and treatment of neurocysticercosis. (2011) Nature reviews. Neurology. 7 (10): 584-94. doi:10.1038/nrneurol.2011.135 - Pubmed
- 6. Jing-LongZhao, Alexander Lerner, Zheng Shu, Xing-Jun Gao, Chi-ShingZee. Imaging spectrum of neurocysticercosis. Radiology of Infectious Diseases Volume 1, Issue 2, March 2015, Pages 94-102 doi:10.1016/j.jrid.2014.12.001
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