Teaching Case

A 50-year-old male patient, known case of type II diabetes mellitus, presented with complaints of sudden onset giddiness and slurred speech followed by weakness involving all four limbs.

CECT brain shows an ill-defined non-enhancing hypodense area involving genu and body of corpus callosum. On MRI, a hyperintense area is noted involving genu and body of corpus callosum on FLAIR, which shows restricted diffusion on ADC.

The corpus callosum is the largest commissural fibre bundle that interconnects both cerebral hemispheres. Anatomically, it is divided into rostrum, genu, body and splenium. Its primary function is to integrate sensory, motor and cognitive information from homologous association areas in the two cerebral hemispheres.

Its ischaemic infarction is not common as it has a rich blood supply from both anterior and posterior systems. Main supplying arteries are pericallosal artery (branch of anterior cerebral artery), posterior pericallosal artery (branch of posterior cerebral artery) and subcallosal and medial callosal arteries (branches of anterior communicating artery) [1]. The pericallosal artery is often the main vascular supply for the body. The subcallosal and medial callosal arteries supply the rostrum and genu. Splenium receives its supply from posterior pericallosal artery.

The main risk factors for developing corpus callosum infarction include atherosclerosis, hypertension, hyperlipidaemia, long-term smoking, diabetes and coronary heart disease [2]. Infarcts most commonly involve splenium followed by body and genu due to the greater incidence of posterior cerebral artery infarcts [3]. Isolated infarcts of the corpus callosum tend to be rare and are usually associated with additional infarcts involving either hemisphere. Clinical features tend to be non-specific and include headache, limb weakness, movement disorders, memory impairment and rarely alien hand syndrome and the classical callosal disconnection syndrome.

CT shows hypodense area involving the affected areas. On MRI, restricted diffusion is the earliest and most sensitive sign. Contrast enhancement is variable and can be seen in the acute phase. Treatment mainly includes antiplatelet therapy, lowering of blood pressure, and reducing the relevant risk factors.