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Lipoma of the Corpus Callosum

Summary

  • Congenital malformation from maldifferentiation of the meninx primitiva, not a neoplasm; usually incidental.
  • Frequently associated with callosal dysgenesis; symptoms, when present, usually reflect the associated malformation rather than the lipoma.
  • Midline pericallosal macroscopic fat, often calcified on CT, suppressing on fat-saturated MRI.

Pathophysiology

  • Abnormal persistence and adipose differentiation of the meninx primitiva, the embryologic precursor of the leptomeninges and subarachnoid space 1
  • Lies in the interhemispheric/pericallosal cistern; pericallosal arteries and, less often, neural tissue may run through it
  • Strong association with agenesis or dysgenesis of the corpus callosum
  • Two morphologic types 2
    • Tubulonodular: bulky, anterior, often >2 cm and calcified; more often associated with callosal dysgenesis and other forebrain malformations
    • Curvilinear: thin, posterior, follows the callosal margin; corpus callosum usually normal or only mildly dysgenetic

Demographics

  • Rare; detected prenatally or incidentally at any age
  • No sex predilection; most patients are asymptomatic

Diagnosis

  • Usually an incidental imaging diagnosis; macroscopic fat is diagnostic and biopsy is unnecessary
  • Reported associations include seizures, headache, and developmental delay — attribute symptoms to the associated malformation rather than the lipoma itself

Imaging

  • Report: morphologic type and extent; corpus callosum formation; associated cortical malformation, interhemispheric cyst, or encephalocele; and the course of the pericallosal arteries through the lesion
  • CT
    • Homogeneous fat attenuation (approximately -50 to -100 HU)
    • Peripheral or nodular calcification, especially in the tubulonodular type
  • MRI
    • T1: markedly hyperintense; sagittal imaging best shows the callosal relationship
    • Fat suppression (fat-sat or Dixon): signal drops out, confirming macroscopic fat
    • T2/FLAIR: hyperintense unless fat-suppressed
    • Chemical-shift artifact at the fat–brain interface; no true diffusion restriction
    • Post-contrast: no internal enhancement, though traversing vessels may enhance; noninfiltrative and should not cause edema
  • Prenatal ultrasound: echogenic midline mass; fetal MRI better characterizes callosal development and associated anomalies

panels-1

  • T1-hyperintense lipoma wrapping around the splenium of the corpus callosum was incidentally indentified.

Treatment

  • None required for a characteristic asymptomatic lesion, and imaging surveillance is unnecessary
  • Surgery is generally avoided because the lesion encases the pericallosal arteries and adheres to neural tissue; reserved for exceptional complications

Differential diagnosis

Differential diagnosis Differentiating feature
Dermoid cyst More heterogeneous, often off-midline; may rupture and scatter fat droplets through the subarachnoid space and ventricles
Teratoma Mixed solid, cystic, fatty, and calcified components with enhancement and mass effect
Falx ossification with fatty marrow Bone windows show cortex and central marrow rather than a cisternal fat mass
Subacute hematoma T1 hyperintensity does not suppress on fat-sat/Dixon; blood-product susceptibility and evolution over time
Thrombosed pericallosal aneurysm Continuity with the artery and residual flow or enhancement; no macroscopic fat

  1. Truwit et al. Pathogenesis of intracranial lipoma: an MR study in 42 patients. 1990. AJNR. American journal of neuroradiology - Open in new tab. ↩

  2. Tart et al. Curvilinear and tubulonodular varieties of lipoma of the corpus callosum: an MR and CT study. 1991. Journal of computer assisted tomography - Open in new tab. ↩