Fact-sheet: Cysticercosis of brain


Updated on 10/03/2018 at 9:22 AM

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Definition

Preventable parasitic infection of the central nervous system caused by a flatworm, the pork tapeworm (or Taenia solium).

Transmission occurs through ingestion of raw or undercooked pork or by ingesting water contaminated with tapeworm eggs.

It is one of the leading causes of epilepsy worldwide.

4 pathologic stages:

  • vesicular
  • colloidal vesicular
  • granular nodular
  • calcified nodular

Clinical features

The most common neurologic signs are:

  • partial or generalized seizures,
  • hemiparesis,
  • headache,
  • psychiatric disturbances,
  • visual disturbances,
  • extrapyramidal signs,
  • intracranial hypertension,
  • vertigo,
  • cranial nerve deficits.

Laboratory findings

Laboratory findings are nonspecific.

In the acute invasive phase, blood eosinophilia may be found.

CSF is often minimally altered, sometimes showing pleocytosis (eosinophils, lymphocytes) and elevated protein levels.

Diagnosis may be established by:

  • imaging (playing a predominant role in the diagnosis of neurologic forms)
  • antibody detection in serum or CSF by ELISA or Western blot.
  • cross-reactions with hydatidosis or schistosomiasis may occur.
  • excisional biopsy: rarely performed in practice.

CT

Four developmental stages of the tapeworm larva underlie CT abnormalities (several stages may coexist in the same patient):

  • Stage I: vesicular stage: (viable larva) difficult to visualize. Cyst with thin, isodense walls. No edema. Hyperdensity within the cyst: protoscolex. Generally no enhancement.
  • Stage II: colloidal vesicular stage: (degenerating larva) cyst with hyperdense fluid content, perilesional edema. Thin, ring-like enhancement.
  • Stage III: granular nodular stage: (dying process) cysts associated with inflammatory changes: loss of margins, nodular enhancement. Perilesional edema.
  • Stage IV: calcified nodular stage: (dead larva) small calcified nodular image, single or multiple.

Lesion location:

  • intraparenchymal (gray matter/white matter junction),
  • intraventricular (fourth ventricle +++),
  • subarachnoid (convexity).
  • basal cisterns.
  • rarely spinal

Shape and size:

  • round or oval cyst, disseminated (miliary) form rare.
  • variable size: from a few millimeters to 2 cm.

MRI

Brain MRI is more sensitive than CT.

Same locations and stages of evolution as on CT:

  • Stage I: vesicular stage: cystic structure isointense to CSF on T1 and T2, containing an eccentric nodule (the scolex, isointense to white matter, is better visualized on T2 FLAIR). No perilesional edema. Occasional mild enhancement of the scolex.
  • Stage II: colloidal vesicular stage: slightly hyperintense to CSF on T1 and T2. Perilesional edema on T2 FLAIR. Thin rim enhancement of the cyst wall or nodule (scolex).
  • Stage III: granular nodular stage: cyst retraction. Decreased perilesional edema. Persistent ring or nodular enhancement.
  • Stage IV: calcified nodular stage: resorption of intracystic fluid, resolution of perilesional edema. Very faint enhancement in some cases. Complete calcification of the lesion: T1 and T2 hypointensity.

Management

Medical treatment: (oral) Albendazole, Praziquantel.

Corticosteroid therapy should always be initiated at the outset to prevent perilesional inflammatory reactions.

Surgical treatment: sometimes required (drainage of parenchymal lesions, ventricular shunting...).

Differential diagnosis

Abcess of brain

Tuberculosis of CNS

Neoplasm

Arachnoid cyst - intracranial

Enlarged Virchow-Robin perivascular spaces