Lesions of the corpus callosum (CC) are a rare oddity and have an estimated prevalence of 0.6-3%. The differential is quite variable and includes neoplastic, demyelinating, traumatic, vascular, hereditary, and infectious etiologies. One such disease cause is Marchiafava-Bignami Disease (MBD). This demyelinating process usually occurs in the setting B1 or B12 deficiency. It is typically attributed to chronic alcohol use, however, also observed in patients with malnutrition. Another etiology is corpus callosum impingement syndrome (CCIS). This is an uncommon sequela of chronic hydrocephalus leading to stretching of the lateral ventricles. We present a case with concurrent processes producing lesions of the CC.   

A 71-year-old man with known normal pressure hydrocephalus, with a ventriculoperitoneal shunt, was originally admitted for one month due to shunt failure and infection. His initial CT head showed hydrocephalus and genu of the corpus callosum (gCC) hypodensity and atrophy. He underwent shunt replacement. On transfer to our facility, repeat CT head revealed “slit like” ventricles and persistent gCC hypodensity. His examination was pertinent for decreased attention, disorientation, bilateral abduction and upgaze paresis, and slowed movements. MRI was obtained which exhibited T2FLAIR hyperintensity of the gCC and dorsomedial thalmi. On further interviewing, it was discovered that the patient had consistently poor oral intake throughout the entirety of his previous hospitalization. Out of concern for thiamine deficiency, the patient was treated with a high dose parenteral thiamine regimen resulting in symptomatic improvement prior to shunt revision.

This case demonstrates two uncommon possible etiologies of lesions of the CC. It seemed CCIS was mostly likely, given his history of prolonged hydrocephalus, re-occurrence with shunt failure, and the presence of the gCC changes prior to malnutrition. However, the uncovering of additional thalamic changes, in the setting of ophthalmoparesis, led to the discovery of the second process, MBD.