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.
On this page:
Epidemiology
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.
Clinical presentation
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
headaches
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.
Pathology
Infection, which leads to extraintestinal 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.
Stages
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 retract further; enhancement persists.
nodular calcified: end-stage quiescent calcified cyst remnant; no oedema.
Location
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
-
ventricles
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.
Radiographic features
Imaging findings depend on the location and stage of infection.
Location
Subarachnoid/intraventricular
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.
In the ventricles, there is often (79%) 2 associated ventriculitis often leading to aqueductal stenosis and hydrocephalus 2.
Parenchymal
Parenchymal cysts usually involve the grey-white matter junction 2.
Stage
Each stage has fairly distinctive imaging features although there is no sharp demarcation between later stages.
Vesicular
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 oedema
Colloidal vesicular
-
cyst fluid becomes macroscopically turbid reflected in altered imaging appearance:
CT: hyperattenuating to CSF
MRI T1: hyperintense to CSF 2
surrounding oedema
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
Granular nodular
oedema decreases
cyst retracts eventually becoming a small enhancing nodule 6
enhancement persists but is less marked 1
Nodular calcified
end-stage quiescent calcified nodule
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
A helpful mnemonic to remember these stages is Vegans Can't Get Neurocysticercosis.
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.
Differential diagnosis
General imaging differential considerations include:
pyogenic cerebral abscess
other parasitic/fungal infection(s)
Unable to process the form. Check for errors and try again.