MR imaging with diffusion-weighted imaging in acute and chronic Wernicke encephalopathy

Abstract

Wernicke encephalopathy is a neurologic disorder that results from thiamine deficiency. It is associated with a classic triad of symptoms consisting of ataxia, ocular motor cranial neuropathies, and changes in consciousness. We report 3 cases of Wernicke encephalopathy in which MR imaging, including diffusion-weighted imaging, was performed at the onset and during follow-up. MR imaging findings were correlated with the clinical status of both the acute and chronic stage of Wernicke encephalopathy.

Fig 1.

Axial FLAIR (A) and diffusion-weighted images (B) from the initial MR imaging examination both demonstrate hyperintensities in the thalami and caudates bilaterally. Axial FLAIR (C) and diffusion-weighted images (D) from the follow-up MR imaging examination 1 year and 10 months later show no abnormal signal intensities in the thalami and caudates bilaterally. Axial FLAIR image (E) shows that there is mild interval increased T2 hyperintense signal intensity in the frontal and parietal white matter.

Fig 2.

Axial FLAIR (A) and diffusion-weighted images (B) from the initial MR imaging examination both demonstrate minimal hyperintensities in the thalami bilaterally (arrows). The hyperintensities are more obvious on the diffusion-weighted image. T2 hyperintensity in the right frontal lobe represents encephalomalacia from a previous injury. Axial FLAIR (C) and diffusion-weighted images (D) from the follow-up MR imaging examination 9 months later show no abnormal signal intensities in the thalami bilaterally. Note the overall volume loss with enlarged sulci and ventricles.

Fig 3.

Axial FLAIR (A) and diffusion-weighted images (B) from the initial MR imaging examination both demonstrate hyperintensities in the thalami bilaterally. The hyperintensities are more obvious on the diffusion-weighted image. Axial FLAIR (C) and diffusion-weighted images (D) from the follow-up MR imaging examination 9 months later show no abnormal signal intensities in the thalami bilaterally. No brain atrophy is found. The abnormal signal intensity in the bilateral front lobes on both the FLAIR and diffusion-weighted images results from the artifact. The follow-up diffusion-weighted image (D) was obtained only using a superoinferior gradient.