Noninvasive neuroradiological examination of WE dates to the 1970s. Early studies used computed tomography (CT) scanning and revealed ventricular enlargement, especially of the third ventricle (Escobar et al.
; McDowell and LeBlanc, 1984
; Mensing et al.
; Shimamura et al.
) but were largely unable to detect edema or focal damage (Gotze et al.
; Gallucci et al.
). The introduction of MR imaging with its exquisite sensitivity to tissue water content and mobility enabled visualization of acute and chronic radiological signs of neuropathology not visible on CT (Antunez et al.
). In some sequences, the MR signal of selective brain structures is hyperintense, indicative of high water content, present in WE because of the edematous nature of the lesions. A direct comparison of CT and MRI in the detection of WE-related neuropathology identified low-density signal abnormalities on CT in the paraventricular regions of thalamus in only 2 of 15 WE patients examined, whereas MRI identified abnormality in this thalamic region in 7 patients of this WE group. Additional affected areas included periaqueductal gray matter in 6 patients and mammillary body shrinkage in 6 WE and 4 of 15 non-WE alcoholic patients. Thus, in vivo
neuroimaging has been instrumental in revealing WE-like neuropathology in alcoholics who do not present with the obvious signs of WE (Sullivan, 2003
; Sullivan and Pfefferbaum, 2005
). Overall, although the sensitivity of MRI in detecting WE was only 53%, the specificity was 93% (Antunez et al.
). Fig. presents an exemplary comparison of CT and different MRI sequences.
Fig. 1 CT and MR images of an acute 35-year-old man with schizophrenia and acute nutritional deficiency-induced WE. (A) Axial CT at the level of the lateral ventricles. (B–E) Axial MR images at a similar level to the CT. (B) A proton density-weighted (more ...)
MR techniques used to enhance visualization of edematous lesions were initially based on T2-weighted late-echo sequences, which are acquired after the majority of the tissue signal has decayed but while the signal of unbound water remains robust (for review, see Bigler, 1996). The most obvious neuroradiological sign of acute WE, regardless of etiology, is bilateral hyperintensity on late-echo MRI, generally occurring in gray matter tissue of the mammillary bodies, anterior and medial nuclei of the thalamus, periventricular gray matter, inferior and superior colliculi (e.g. nonalcoholics: Doraiswamy et al.
; Chu et al.
; Unlu et al.
, 2006; Zhong et al.
) (alcoholics: Schroth et al.
) and occasionally cererbellum (Shear et al.
; Nicolas et al.
; Sullivan et al.
; Bae et al.
). These observations are consistent with postmortem reports (e.g. Torvik et al.
; Harper and Kril, 1988
; Kril et al.
; Baker et al.
). The bilateral distribution of the neuropathology may contribute to the severity of the clinical signs and symptoms. Although the pons is not usually implicated in WE, an MR study examining T2 relaxation time, a measure of interstitial fluid reflecting axonal and myelin integrity, provided evidence of excessive fluid in the central pons of patients with alcoholic WKS (Sullivan and Pfefferbaum, 2001
). Predictors of prolonged relaxation time in non-KS alcoholics in this study were hematological measures of nutritional status, e.g. macrocytic anemia and cognitive fluency.
The development of the MR fluid-attenuated inversion recovery (FLAIR) sequence provided significant improvement over the conventional T2 approach by incorporating additional T1 contrast mechanisms. An advantage of the FLAIR approach is that it essentially eliminates only signal with T1 characteristics of CSF, including in regions of non-tissue CSF, such as sulci and ventricles, and therefore enhances the conspicuity of the signal in boggy, edematous tissue. Several case studies have published in vivo
FLAIR images of acute WE (Maeda et al.
; Ashikaga et al.
). An early study of a woman with hyperemesis gravidarum revealed high signal intensity of the mammillary bodies and hypothalamus; following thiamine treatment, although the high signal intensity resolved, the mammillary bodies shrank (Maeda et al.
). A series of six cases of nonalcoholic WE studied with FLAIR revealed hyperintense signal in the tissue around the aqueduct, third ventricle, floor of the fourth ventricle, anterior ventricular caps and medial thalami; follow-up examination noted recovery in the four cases without cortical damage but not in the two cases with such damage (Zhong et al.
MR diffusion-weighted imaging (DWI), in which signal from freely diffusing water is suppressed, is another MRI method that has proved sensitive to the detection of WE brain pathology. An example of WE lesions with DWI is presented in Fig. . Paradoxically, the edematous lesions of WE, which would be expected to have high levels of diffusivity and have their signal suppressed with DWI, are instead hyperintense. This is an example of the ‘T2 shine-through effect’, in which tissue with long T2 value is bright (Koch and Norris, 2005
); thus, the bright signal, rather than representing low diffusivity, reflects the opposite. In addition to the periventricular and thalamic tissue abnormalities typically identified with WE (Halavaara et al.
; Unlu et al.
), one case study concluded that bright signal on DWI was caused by abnormally low diffusivity in the cerebellum. Even though the diffusivity abnormality in the cerebellum resolved with thiamine repletion, noted at a 3-month follow-up study, associated motor impairment persisted (Lapergue et al.
). DWI-increased signal intensity, confirmed as decreased diffusivity with apparent diffusion coefficient (ADC) images, in affected brain regions has been reported in two studies of acute WE (Halavaara et al.
; Lapergue et al.
). Because interpretation of DWI can be confounded by the T2 shine-through effect, DWI is probably of greatest value when accompanied by ADC imaging for quantitative assessment of the water diffusion. Together, the two techniques provide a method for characterizing the evolution of WE lesions from early edematous high diffusivity through later atrophic low diffusivity.
Figures and present FLAIR images of an acute WE case, a 35-year-old man with schizophrenia, found lethargic and confused in his apartment. He had suffered weight loss from inadequate nutrition. Examination revealed failure of horizontal gaze and ataxia of gait; management included daily doses of intravenous thiamine 100 mg. This case is striking because all neuropathological indices are present, and the lesions are bilateral and visible as signal hyperintensities. The structures affected in this case of WE are the mammillary bodies, periventricular gray matter, thalamus, inferior colliculi and fornix.
Fig. 2 Three contiguous FLAIR images (5 mm thick with a 2.5 mm skip) of the acute WE case in Fig. . Note the hyperintense signal in the mammillary bodies and colliculi (left), periventricular gray matter (middle), and fornix and thalamus (right). (more ...)