Neurocysticercosis (NCC) 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 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 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 faeces 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 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 are 3,4:
- subarachnoid space over the cerebral hemispheres (can be very large): most common location
- parenchyma: second most common location, frequently seen near the grey matter–white matter junction 4
- basal cisterns
- may be "grape like" (racemose): most lack an identifiable scolex
- usually solitary cysts
- 4th ventricle most frequent
Typically the parenchymal cysts are small (1 cm) whereas the subarachnoid cysts can be much bigger (up to 9 cm): differential therefore being arachnoid cyst.
It is the most common cause of epilepsy in endemic areas (Southeast Asia, South America) with progression through the four stages taking anywhere between 1 to 9 years.
Imaging findings depend on location and stage of infection.
When in the subarachnoid space/interventricular, 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: hyperattenuating to CSF
- MRI T1: hyperintense to CSF 2
- surrounding oedema
- cyst and the wall become 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
- end-stage 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
- 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
Infections of the central nervous system
- classification by aetiology
- eastern equine encephalitis
- enterovirus rhomboencephalitis
- flavivirus encephalitis
herpes virus family
- herpes simplex virus 1 (HSV-1) encephalitis
- herpes simplex virus 2 (HSV-2) encephalitis
- varicella zoster virus (VZV) encephalitis
- Epstein-Barr virus (EBV) encephalitis
- cytomegalovirus (CMV) encephalitis
- human herpesvirus 6 (HHV-6) encephalitis
- HIV CNS manifestations
- HTLV-1-associated myelopathy
- JC virus
- measles encephalitis
- Nipah virus (NiV) encephalitis
- rabies encephalitis
- CNS listeriosis (Listeria monocytogenes)
- CNS nocardiosis (Nocardia spp)
- CNS tuberculosis (Mycobacterium tuberculosis)
- Lyme disease (Borrelia burgdorferi)
- neurosyphilis (Treponema pallidum)
- Rocky Mountain spotted fever (Rickettsia rickettsii)
- cerebral amoebiasis
- cerebral malaria (Plasmodium falciparum)
- cerebral sparganosis (Spirometra mansonoides)
- neurocysticercosis (Taenia solium)
- neurohydatidosis (Echinococcus spp)
- neurotoxoplasmosis (Toxoplasma gondii)
- others or those with possible infectious aetiologies
- classification by location
- meninges and ventricular system
- brain parenchyma, brainstem, and spinal cord
- classification by aetiology