Non-alcoholic Wernicke's encephalopathy: broadening the clinicoradiological spectrum

Abstract

Wernicke's encephalopathy (WE) is a serious neurological disorder secondary to thiamine deficiency. Improved recognition by radiologists and allied health providers of the different clinical settings and imaging findings associated with this emergency can optimise the management of this condition and help prevent its severe consequences. The aim of this study is to illustrate the broad clinicoradiological spectrum of non-alcoholic WE, while emphasising atypical MRI findings.

Figure 1

Male patient, 63 years old, with persistent vomiting, presented ocular disturbances and vertigo after surgery for gastric adenocarcinoma. Coronal fluid-attenuated inversion recovery images show bilateral and symmetrical hyperintense lesions bordering the third ventricle in the dorsomedial thalami and the periaqueductal region (arrows).

Figure 2

37-year-old female patient with total colectomy due to ulcerative rectocolitis presented severe pancreatitis and vomiting and manifested vertical and horizontal nystagmus 1 week after surgery. T₁ and T₂ fast spin-echo (FSE) images disclose no abnormalities in the mamillary bodies (not shown), while sagittal enhanced T₁ weighted image shows conspicuous enhancement of the mamillary bodies (arrow).

Figure 3

Male patient, 17 years old, with a history of bone marrow aplasia and repeated infections, evolved with persistent vomiting for 2 months and acute onset of mental confusion. The first examination shows no abnormalities on the axial T₂∗ image (a), but the axial enhanced T₁ weighted image (b) shows enhancement of the mamillary bodies (arrows). Follow-up examination was performed after 1 month: the axial T₂∗ image (c) now clearly demonstrates hypointensity in the mamillary bodies (arrows), assigned to haemosiderin deposition, whereas the corresponding axial enhanced T₁ image (d) demonstrates reversal of mamillary body enhancement.

Figure 4

27-year-old female patient with a history of depression and anorexia nervosa. She developed acutely altered mental status; MR examination was performed after 3 days. High signal intensity was noted at the caudate nuclei (arrowheads) on axial fluid-attenuated inversion recovery (a) and axial T₂ weighted images (b).

Figure 5

Same patient as Figure 4. Axial DWI (a, b) and corresponding apparent diffusion coefficient maps (c, d) show bilateral and symmetrical restricted diffusion in caudate nuclei and perirolandic cortex 3 days after onset of clinical picture.

Figure 6

Female patient, 52 years old, after surgery for rectal adenocarcinoma, submitted to chemotherapy and on total parenteral nutrition, presented acutely with vertigo, abnormal eye movements and altered consciousness. Axial fluid-attenuated inversion recovery images (a, b) show symmetrical hyperintensity in the posterior putamina (arrows in a), dorsomedial thalami (arrowheads in a) and perirolandic cortex (arrows in b).

Figure 7

Same patient as in Figure 6. Axial fluid-attenuated inversion recovery images (a–d) show symmetrical hyperintensities involving the prepositus hypoglossal nuclei (arrows in a), medial vestibular nuclei (arrows in b), facial nuclei (arrows in c), abducens nuclei (arrowheads in c), mid-brain tectum and periaqueductal grey matter (arrows in d).

Figure 8

Same patient as in Figure 6. DWI obtained 2 days after the first symptoms failed to disclose any abnormalities (not shown). Follow-up DWI (a) and corresponding apparent diffusion coefficient map (b) obtained 7 days after clinical onset show true restricted diffusion in the putamina (arrows), attributed to cytotoxic oedema, where the high signal observed in the dorsomedial thalami (asterisks) is not accompanied by low signal on ADC map (possibly due to vasogenic oedema).

Figure 9

Same patient as in Figure 6. Axial T₁ post-contrast images disclose enhancement in the periaqueductal region (thin arrow), tectal plate (large arrow) and perirolandic cortex (arrowheads).