Wernicke’s encephalopathy is a neurologic disorder with acute onset, characterised by the triad of ocular abnormalities, ataxia, and a confused state. It is caused by a thiamine deficiency due to poor oral intake in chronic alcoholics, food refusal, recurrent vomiting in a pregnant patient , tumours of the gastrointestinal tract, gastroplasty for obesity, psychogenic refusal of food, anorexia nervosa, prolonged infectious-febrile disease, voluntary food starvation, chronic uremia and parenteral therapy. If left untreated, severe amnesic deficits, Korsakoff psychosis, and even death may follow the acute phase of the disease. Ocular symptoms and ataxia were more frequently seen in the alcohol abuse group [1, 2].
The anatomic regions most frequently involved by symmetric lesions were the medial thalami and the periventricular area of the third ventricle. These areas represent regions where maintenance of cellular osmotic gradients is strictly related to physiologic levels of thiamine concentration and where any reduction in thiamine may determine early symmetric metabolic breakdown, as easily evidenced by MR as cytotoxic oedema.The lesions of the thalamus and periventricular region of the third ventricle were always associated with other alterations typical of the disease [2].
On MR imaging, the pathologic alterations described above are typically seen as bilateral and symmetrical T2 and FLAIR hyperintensities in the thalami, mammillary bodies, tectal plate and periaqueductal area. Signal intensity alterations in the dorsal medulla and the pons, cerebellar dentate nuclei, red nuclei, the substantia nigra of the midbrain, cranial nerve nuclei, the vermis and the paravermian regions of the cerebellum, the corpus callosum, the fornices, the head of the caudate nucleus, and the frontal-parietal cortex represent atypical MRI findings; they are almost always found in association with the typical findings. In the diagnosis of acute Wernicke’s encephalopathy DWI (diffusion-weighted imaging), detecting changes in water diffusion associated with cellular dysfunction is surely a valuable additional imaging sequence. The lesions can show hyper intensity on DWI images and reduced, normal, or increased ADC (apparent diffusion coefficient) values. Cerebellar signal intensity alterations can be observed in both alcoholic and nonalcoholic patients. Gadolinium administration can be a useful tool to identify Wernicke's encephalopathy cases with a negative MRI. Contrast-enhanced T1-weighted images point out areas with disrupted blood-brain barrier and enhancement can be seen in about 50% of cases. Strong enhancement of the mammillary bodies, for instance, can be the only sign of the disease and is more frequent in chronic alcoholics [2, 3].
The treatment of suspected or manifest WE is based on the administration of thiamine [3].