Wernicke’s Encephalopathy: Expanding the Diagnostic Toolbox

Abstract

Wernicke's encephalopathy (WE) is a life threatening neurological disorder that results from thiamine (Vitamin B1) deficiency. Clinical signs include mental status changes, ataxia, occulomotor changes and nutritional deficiency. The conundrum is that the clinical presentation is highly variable. WE clinical signs, brain imaging, and thiamine blood levels, are reviewed in 53 published case reports from 2001 to 2011; 81 % (43/53) were non-alcohol related. Korsakoff Syndrome or long-term cognitive neurological changes occurred in 28 % (15/53). Seven WE cases (13 %) had a normal magnetic resonance image (MRI). Four WE cases (8 %) had normal or high thiamine blood levels. Neither diagnostic tool can be relied upon exclusively to confirm a diagnosis of WE.

The Whole Spectrum of Alcohol-Related Changes in the CNS: Practical MR and CT Imaging Guidelines for Daily Clinical Use

“…It is important to know that hypovitaminosis is frequently not associated with alcohol abuse but nonetheless results in "typical" visible morphological changes [23]. Therefore, for example, up to 81 % of a cohort of patients with Wernicke encephalopathy (see below) did not have a history of alcohol abuse [24]. Differences in the clinical manifestation of the disease depending on whether there is an alcoholic or non-alcoholic genesis have been described [25].…”

“…Vegetative dysregulation typically accompanies this triad. HIV infection is a risk factor for development of the disease [11,23,24]. The main symptoms of Korsakoff syndrome (KS) are anterograde amnesia and retrograde amnesia going back over multiple years in some cases, lack of drive, and impairment of executive functions.…”

“…Severely impaired consciousness is rare. WE becomes chronic KS in 56 % to 81 % of cases and can thus be viewed as an acute form of KS [24]. WE and KS are based on a lack of energy in the CNS caused by a thiamine deficiency that occurs already after approximately 18 days in the case of an absolute cessation of absorption [23].…”

“…CT imaging is usually not productive. Patients should ideally be examined with MRI [24,30]. Focal cerebral edema and in severe cases blood-brain barrier disruption as well as restricted diffusion can be detected on MRI in both diseases.…”

Wernicke’s Encephalopathy Due to Hyperemesis Graviderum : A Rare Presentation

“…Lack of thiamine also affects major energy consumer myocardium and patient may develop cardiomegaly, heart failure. Cardiac abnormalities are one of the most important trigger of death in Wernicke's encephalopathy [1][2][3] .…”