What is the role of MRI in the diagnosis of Wernicke encephalopathy (WE)?

Updated: Nov 20, 2018
  • Author: Philip N Salen, MD; Chief Editor: Andrew K Chang, MD, MS  more...
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Thiamine is a cofactor of several enzymes involved in glucose metabolism and cerebral energy utilization, and its depletion results in the neuronal damage as seen on MRI, including T2 and fluid-attenuated inversion recovery hyper-intense signaling in the mammillary bodies, periventricular thalamus, and periaqueductal gray matter, as well as diffusion-weighted imaging to differentiate vasogenic from cytotoxic edema. [2]

The sensitivity and specificity of MRI has been reported at 53% and 93% with a positive predictive value of 89%; in other words, MRI is better at confirming the diagnosis of WE than ruling it out. [1]  MRI offers a technique to make a definitive diagnosis antemortem, but the sensitivity is poor, and obtaining an MRI for this indication is typically impractical and unnecessary in the emergency department (ED). [5]

Although the clinical evidence for the utility of MRI is based on a study in which the sample size was small, the reported sensitivity of MRI was 53% and the reported specificity was 93%, for acute and chronic WKS. Because of the low sensitivity of MRI for WE, particularly an acute presentation, and because many patients with WE may not exhibit diagnostic features on MRI, normal MRI results does not preclude the diagnosis of acute illness. [13]

The appearance of acute WE on MRI demonstrates abnormal hyper-density of the mammillary bodies and periaqueductal gray matter with associated abnormal enhancement on T1-weighted images. [16] In chronic WE and WKS, radiographic imaging, especially MRI, may be normal or may show mamillary body, cerebellar, and cerebral shrinkage, as well as symmetrical, low-density abnormalities in periventricular areas, the diencephalon, and the midbrain. [13] Such symmetrical lesions are uncommon in other cerebral encephalopathic disorders and are suggestive of WKS. [13]

Morphometric studies of MRI imaging confirm that patients with WKS show excessive mammillary body and cerebellar shrinkage, indicating that these are highly specific MRI findings for this kind of encephalopathy. [13]

The image below shows brain morphologic studies as demonstrated on MRI. A 60-year-old man presented with bilateral gaze-evoked nystagmus, severe ataxia, and memory impairment. Brain fluid-attenuated inversion recovery (FLAIR)–weighted MRI shows concurrent cytotoxic and vasogenic edema patterns. This case demonstrates cytotoxic and vasogenic edema that may occur at the same time in WE. These findings may result from different vulnerability of brain regions to thiamine deprivation and the corresponding time delay between the development of lesions. [17]

This MRI shows typical high signal intensities (SI This MRI shows typical high signal intensities (SIs) in the medial thalamus (A), periaqueductal gray (B), mamillary bodies (C), cerebellar vermis (B, C, D), and paravermian superior cerebellum (D). All the lesions represent high SIs on the DWI (E–H). The ADC images of the cerebellar vermis (K, L) and paravermian superior cerebellum (L) show low SIs (arrowheads), whereas other described areas (I, J) show iso-SIs (arrows). Image courtesy of Neurology. Apr 8 2008;70(15):e48.

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