Teaching Case

A 54-year-old female patient presented with acute onset confusion and mental sluggishness. Apart from a delay in psycho-motor responsiveness, no other neurological features were present. She was diagnosed with alimentary B12 deficiency a month before the onset of the current episode.

Axial DWI picture (Figure 1a) with corresponding ADC axial slice (Figure 1b) show the presence of bilateral medial thalamic hyperintensities without diffusion restriction. Figure 1c present the DWI slice of the same patient one month before, where, retrospectively, subtle bilateral medial thalamic hyperintensities can be observed.

In the T2W axial image (Figure 2a) of the same patient bilateral medial thalamic hyperintensities are seen. The findings were not present in the prior examination (Figure 2b).

On the axial T1W after intravenous gadolinium administration, enhancement of the mammillary bodies is observed (Figure 3).

Wernicke´s Encephalopathy (WE) is a neurologic disorder that results from thiamine (vitamin B1) deficiency. The classical clinical triad is characterised by acute confusion, ophthalmoplegia, and ataxia. [1]. However, the more frequent clinical symptoms, such as loss of appetite or irritability, are frequently nonspecific. [2] In a retrospective post-mortem study, the WE was found to be misdiagnosed in up to 80% of the patients. [3] Consequently, an accurate differential diagnosis of the neuroimaging findings is essential.

Brain CT has lower sensitivity compared to MRI in the acute setting of WE. [4-6]

Brain MRI is the most critical examination in the diagnosis, showing T2W hyperintensities in mammillary bodies, medial aspects of the thalami, tectal plate, periaqueductal grey matter, and dorsal medulla. [4]

The medial thalami and the periventricular regions are considered typical MR findings, while the atypical findings are represented by alterations in the cerebellum, basal ganglia, cortex and corpus callosum splenium. [5]

Similar bilateral thalamic abnormalities can be seen in a myriad of pathologies. Metabolic conditions such as osmotic myelinolysis, vascular abnormalities such artery of Percheron infarction or bilateral deep cerebral venous thrombosis, primary gliomas or lymphomas, flavivirus, and Creutzfeldt-Jakob Disease are all included in the differential. [6]

Signal intensity alterations with contrast enhancement in the mammillary bodies is a helpful differential tool and may be the only sign of WE. [5]

Alcohol abuse is frequently associated with thiamine deficiency. However almost half of the cases have other etiologies. [1] Contrast enhancement of the mammillary bodies and thalamus has been reported to be more typical of patients with alcohol abuse, while signal intensity alterations in the infratentorial location were more frequently seen in non-alcoholic patients. [7] Other studies found no differences between the two groups. [8]

In our patient, after reporting the possibility of WE, the patient was found to have vitamin B1 deficiency associated with vitamin B6 deficiency. The nutritional supplementation already corrected the B12 deficiency. Patient's alcohol consumption was anecdotal, and the extensive imaging and endoscopic evaluation did not show evidence of malignant disease. It was then assumed that the deficits were of dietary origin. One week after the supplementation of the deficiencies, the patient presented a marked clinical improvement.

Written informed patient consent for publication has been obtained.