A Rare Case of Marchiafava-Bignami Disease With Reversible Splenial Lesion

Abstract

Individuals with a history of chronic alcohol consumption can develop Marchiafava-Bignami disease (MBD), a rare neurological disorder that is thought to occur secondary to thiamine deficiency and alcohol-induced brain damage. It is characterized by the toxic demyelination and necrosis of the corpus callosum. We report the case of a 42-year-old man who developed acute-onset altered sensorium and irrelevant speech output associated with ataxia. The clinical presentation raised a suspicion of MBD, although it was not a top differential diagnosis initially. Magnetic resonance imaging revealed significant demyelination of the splenium of the corpus callosum, confirming the suspicion and prompting immediate intervention aimed at addressing both the neurological manifestations and the possible underlying thiamine deficiency. Relevant history of significant alcohol consumption further supported this diagnosis. Following the initiation of thiamine supplementation and supportive care, the patient exhibited gradual improvement in neurological function, eventually leading to a complete clinical recovery and resolution of radiological findings, suggestive of the type B spectrum of the disease. This report highlights the importance of clinical evaluation and neuroimaging in the diagnosis, treatment, and prognostic stratification of patients with MBD.

Keywords: alcohol related complications; corpus callosum lesion; marchiafava-bignami disease (mbd); splenium of the corpus callosum; thiamine or vitamin b1 deficiency.

Figure 1. EEG

The EEG capture shows intermittent slowing in the theta range.

Figure 2. MRI Brain

A) The diffusion-weighted imaging (DWI) sequence shows restricted diffusion at the splenium of the corpus callosum (red arrow), possibly suggestive of transient intra-myelinic edema in this case. This pattern is consistent with partial corpus callosum involvement typical of Marchiafava-Bignami disease (MBD) type B. B) The corresponding apparent diffusion coefficient (ADC) map shows restricted diffusion at the splenium of corpus callosum (red arrow).

Figure 3. MRI Brain

A) The Fluid-Attenuated Inversion Recovery (FLAIR) sequence—sagittal view—shows a hyperintense lesion at the center of the splenium of the corpus callosum, sparing the peripheral fibers—"sandwich sign" (red arrow)—signifying possible transient intra-myelinic edema. B) The FLAIR sequence—axial view—shows a hyperintense lesion at the splenium of the corpus callosum (red arrow).

Figure 4. MRI Brain follow-up scan after six weeks of the initial scan.

A) The diffusion-weighted imaging (DWI) sequence shows complete resolution of the prior restricted diffusion lesion at the splenium of corpus callosum seen in Figure 2A. B) The corresponding apparent diffusion coefficient (ADC) map shows complete resolution of the prior restricted diffusion lesion at the splenium of corpus callosum seen in Figure 2B.

Figure 5. MRI Brain follow-up scan after six weeks of the initial scan.

A) The Fluid-Attenuated Inversion Recovery (FLAIR) sequence (sagittal view) shows complete resolution of the prior hyperintense lesions involving the splenium of the corpus callosum seen in Figure 3A. B) The FLAIR sequence sagittal view (zoomed image) shows complete resolution of the prior hyperintense lesions involving the splenium of the corpus callosum seen in Figure 3A.