Cysticercosis

Infectious diseases

General description

Cysticercosis is caused by Tania solium after fecal-oral contamination of infective embryos that cross intestinal mucosa and disseminates typically into brain and muscles.

Imaging studies reveal varying findings based on the viability and degeneration of the parasite. The progression of the infection can be categorized into four known stages:

  1. Vesicular stage
  2. Vesicular colloidal stage
  3. Granular nodular stage
  4. Nodular calcified stage

Vesicular stage

In the vesicular stage, the parasite resides quiescently in the brain parenchyma as a small nonenhancing cyst without edema in the surrounding white matter. The presence of the scolex in the cysts may be observed as a target or dot in a hole appearance.

Vesicular colloidal stage

In the vesicular colloidal stage, the death of the scolex causes disruption of the cyst wall resulting in an intense inflammatory reaction. Proteins from inflammatory reactions and proteins from parasite carcasses accumulate in the cyst contents and become debris.

Granular nodular stage

In the granular nodular stage, the cysts retract and form granulation nodules accompanied with calcification and surrounding gliosis.

Nodular calcified stage

The nodular calcified stage is the final stage of neurocysticercosis, in which nodular calcification occurs and edema is no longer seen.

Vesicular stage

  • Anywhere in the brain
Central
Plain CT
Water attenuation
T1WI
Hypointensity
T2WI
Hyperintensity
Water intensity
Nodular
T2WI
Hypointensity
Nodular
Peripheral
Plain CT
High attenuation
T1WI
Hyperintensity
DWI
Hyperintensity
CE T1WI
No enhancement

Vesicle of the cysticercosis is composed of parasite body, retention fluid, and surrounding membrane. Fluid component shows T2WI hyperintensity same as cerebrospinal fluid.

A nodule within the cyst represents viable parasites, which exhibit diffusion restriction on imaging studies.

Vesicular colloidal stage

  • Anywhere in the brain
Central
Plain CT
Water attenuation
T1WI
Hypointensity
T2WI
Hyperintensity
Water intensity
Nodular
Peripheral
Plain CT
High attenuation
T1WI
Hyperintensity
T2WI
Hypointensity
DWI
Hyperintensity
Ring shaped
Nodular
CE T1WI
Enhancement

When degenerated parasites release metabolic components that cross the blood-brain barrier, they provoke an inflammatory reaction around the lesion. Imaging studies then reveal a contrast effect and edema, indicative of inflammation.

DWI displays nodular hyperintensity within a hypointense vesicle.

Granular nodular stage

  • Anywhere in the brain
Central
Plain CT
Water attenuation
T1WI
Hyperintensity
T2WI
Hyperintensity
DWI
Hyperintensity
Ring shaped
Nodular
Peripheral
Plain CT
Calcified attenuation
Nodular
Peripheral
T1WI
Isointensity
T2WI
Hypointensity

The degeneration of the vesicle leads to calcification within the cyst, with the nodule also exhibiting calcification. CT imaging is effective in showing calcification. On MRI, these calcified areas appear as isointense to brain parenchyma on T1WI and display iso-hypointensity on T2WI.

DWI reveals hyperintensity in the vesicular component, indicative of the viscosity of the internal content.

Nodular calcified stage

  • Cerebrum
    Cerebral white matter
    Subcortical white matter
  • Cerebellum
  • Caudate nucleus
  • Putamen
  • Globus pallidus
  • Thalamus
  • Brainstem
  • Subarachnoid space
  • Ventricle
Multiple
Plain CT
Calcified attenuation
T1WI
Hypointensity
T2WI
Hypointensity
T2*WI
Hypointensity
SWI
Hypointensity

CT shows multiple calcified nodules in brain parenchyma. T2WI and T2*WI reveal multiple hypointensities in the same region.