Wernicke's encephalopathy

A post about Wernicke's at Renal Fellow Network prompted this literature search.


This article covers CT and MRI findings:

CT and above all MRI of the brain play a fundamental role in diagnosing the condition and ruling out other diseases. MRI is the most sensitive technique and is required in all patients with a clinical suspicion of Wernicke’s encephalopathy. Medial thalami, mamillary bodies, tegmentum, periaqueductal region, and tectal plate are typical sites of abnormal MRI signal. The dorsal medulla, red nuclei, cranial nerve nuclei, cerebellum, corpus callosum, frontal and parietal cerebral cortex are less common sites of involvement although they are more frequently affected in nonalcoholic patients. Paramagnetic contrast material may help to identify lesions not otherwise visible.

This review of WE focuses on imaging findings but also comments on clinical criteria and pathophysiology:

In view of the poor diagnostic performance of the classical triad, new classification criteria have been proposed. These criteria require two of four items including dietary deficiencies, oculomotor abnormalities, cerebellar dysfunction, and an altered mental state or mild memory impairment [13]...

Alcoholism does not directly cause thiamine deficiency, although it may induce such deficiency because of its frequent association with malnourishment. More specifically, the low thiamine absorption rate at the mucosal level, the impaired hepatic function, and the alcohol-related raised thiamine metabolism together may lead to the development of chronic thiamine deficiency [14]. Thiamine-deficient membranes are unable to maintain osmotic gradients, which results in the swelling of intra- and extracellular spaces.

From the discussions in this and other reviews it is apparent that the mechanisms by which thiamine deficiency produce the brain lesions of WE are multifactorial and poorly understood.


This fascinating review explores the controversial and sometimes confusing overlaps between WE, Korsakoff Syndrome (KS) and non-thiamine related alcohol dementia.


This review highlights the increasing recognition of WE as a complication of bariatric surgery.


This article reviews several aspects of the clinical findings, natural history and pathology of WE and KS. It emphasizes the under-diagnosis of WE. This under-diagnosis is due to the fact that only 10-15% of patients present with the classic triad (eye findings, ataxia and mental status changes).


This case series illustrates that WE may be associated with a characteristic acid-base disturbance, combined respiratory alkalosis and wide anion gap metabolic acidosis such as is seen in salicylate intoxication.


Here is a review of the emergency prevention and management of WE in acutely ill patients emphasizing common pitfalls. The discussion of early recognition deals with non-WE presentations of thiamine deficiency such as cardiovascular collapse, heart failure, lactic acidosis and acute abdominal symptoms. Also listed are non-alcohol related conditions now known to be associated with WE: hyperemesis gravidarum, TPN without adequate thiamine supplementation and post-bariatric surgery states. The pathophysiology and biochemistry of WE are described as complex, and the brain lactate accumulation mentioned in the post at Renal Fellow Network is probably but one of several mechanisms of injury.


A 2007 review from Lancet Neurology cites an even wider variety of non-alcohol scenarios that can be associated with WE including fad diets and nutritional imbalances of various sorts, magnesium deficiency (it may induce refractoriness to administered thiamine) and various situations in cancer patients. The review makes the point which, though obvious, bears mention, that WE cannot reliably distinguished from drunkenness. The optimal route for thiamine administration is IV. Although deemed controversial in some of the other reviews this one makes more specific statements about dosing. 100 mg IV daily is common practice, and while this may be appropriate for prophylaxis in at risk patients, the review recommends 500 mg IV tid for patients with strongly suspected or established WE to prevent KS, other brain damage or death. (A banana bag may not be enough!).


The profile of WE has changed. During my training, as now, the diagnosis of WE was primarily clinical. Confirmatory diagnostic testing, however has changed. Then it was done by blood testing (thiamine levels or red cell transketolase assays) whereas now MRI is the diagnostic modality of choice. Neither is useful in the acute situation, as thiamine repletion must begin in the emergency setting before confirmatory test results are available. The epidemiology has changed. Because parenteral thiamine administration in the ER has become almost knee-jerk in alcoholic patients, we may be seeing less alcohol-related WE in comparison to other circumstances such as hyperemesis gravidarum, post-bariatric surgery states and other instances of disturbed nutrition.