-         Complete agenesis

-         Partial agenesis 

The corpus callosum is a thin band of white matter, which is difficult to demonstrate sonographically. It is only well visualized on mid-sagittal or mid-coronal views of the brain and requires optimal angles of insonation to demonstrate.








Interhemispheric cyst,high-riding 3rd ventricle




Sunburst appearance of gyri




 Interhemispheric cyst,high-riding 3rd ventricle










Interhemispheric fissure adjoins the 3rd ventricle





Colpocephaly (dilatation of the occipital horn of the lateral ventricle).



Callosal Agenesis – absent cingulated gyrus and pericallosal artery

Normal Corpus Callosum – normal pericallosal artery



Normal cingulate gyral pattern.

Dysgenesis of the cingulate gyrus with characteristic radial orientation of the sulci

Normal corpus callosum, pericallosal (PC) and callosomarginal (CM)arteries.

Agenesis of the corpus callosum with a "sunburst" gyral pattern and non visualization of the pericallosal or callosomarginal arteries



Postnatal MRI scan



o       Lipoma or interhemispheric cysts (preventing the progression of callosal axons as they are median structures) (7).

o       Late remodelling abnormality of callosal connections causing thinning of the corpus callosum may occur in utero or even at birth after severe asphyxia.

o       Prenatal ultrasound examination can usually diagnose CACC from 22 weeks onwards (8).

o       Absence of the cavum septi pellucidi, upward displacement and enlargement of the third ventricle

o       Enlarged occipital horns (colpocephaly) of the lateral ventricles,

o       separated and enlarged anterior horns,

o       enlarged interhemispheric spaces are the key indirect signs of CACC.

o         Color Doppler can also show the loss of the semicircular loop of the pericallosal artery (8)






The caudal portion of the corpus callosum (splenium and body) are missing to various degrees.

Partial agenesis affects only the posterior part of the corpus callosum.

o       Indirect signs are lacking and prenatal diagnosis is therefore more difficult (9).

o       Hypoplasia occurs as a result of late destruction of the corpus callosum (10) owing to a metabolic, infectious or ischemic origin.


Amino acid metabolism

non-ketotic hyperglycinemia

maternal phenylketonuria

methyl malonic acidemia


pyruvate dehydrogenase deficiency

pyruvate decarboxylase deficiency

fumarase deficiency


Zellweger syndrome

Refsum syndrome


Other metabolic

glutaric acidemia

congenital disorder of glycosylation

3-hydroxyisobutyric aciduria

Ante or postnatal ischemic
or infectious events

necrotizing enterocolitis

severe birth asphyxia

antenatal cerebral vascular infarction

fetal toxoplasmosis or rubella


trisomy 8, 13, 18, 21

Other syndromes

Menkes syndrome

Smith-Lemli-Opitz syndrome

Shapiro syndrome

fetal alcohol syndrome

acrocallosal syndrome

septo-optic dysplasia

ectodermal dysplasia

Other cerebral

defect of gyration pattern, microgyria


anomaly of cerebral white matter

cerebellar dysplasia

interhemispheric cyst

Paupe A, Bidat L, Sonigo P et.al. Prenatal diagnosis of hypoplasia of the corpus callosum in association with non-ketotic hyperglycemia.      Ultrasound Obstet Gynecol 2002;20:616-619




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