Neurocysticercosis

Dr Tee Yu Jin and A.Prof Frank Gaillard et al.

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 
  • headaches
  • hydrocephalus
  • 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):

  1. vesicular: viable parasite with intact membrane and therefore no host reaction. 
  2. 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.
  3. granular nodular: edema decreases as the cyst retract further; enhancement persists.
  4. 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
  • 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.

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.

In the ventricles, there is often (79%) 2 associated ventriculitis often leading to aqueductal stenosis and hydrocephalus 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 edema
  • cyst and the wall become thickened and brightly enhances
  • scolex can often still be seen as an eccentric focus of enhancement
  • edema decreases
  • cyst retracts
  • enhancement persists but is less marked 1
  • end-stage quiescent calcified cyst remnant
  • 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

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:

Infections of the central nervous system
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Article information

rID: 1724
Synonyms or Alternate Spellings:
  • Neurocisticercosis
  • Neurocysticercosis (NCC)
  • Racemose cisticercosis

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Cases and figures

  • Figure 1: life cycle
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  • Case 1: hydrocephalus due a vesicular stage lesion
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  • Case 2: colloidal vesicular stage
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  • Case 3: vesicular/coloidal vesicular
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  • Case 4: calcified lesions with minor edema
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  • Case 5: nodular calcified stage
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  • Case 6: nodular calcified stage
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  • CET1W  AXIAL

The...
    Case 7: multiple lesions affecting posterior fossa
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  • Case 8
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  • FLAIR Axial
    Case 9: intraventricular
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  • Case 10
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  • Case 11: disseminated
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  • Case 12
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  • Case 13: intraventricular cysticercosis
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  • Case 14
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  • Case 15: on vesicular stage
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  • CET1W SAGITTAL

M...
    Case 16: posterior fossa
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  • Case 17: disseminated
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  • Case 18
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  • Case 19
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  • Case 20: vesicular neurocysticercosis with subacute infarct
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