Comprehensive review of Wernicke encephalopathy: pathophysiology, clinical symptoms and imaging findings

Abstract

Wernicke's encephalopathy (WE) is a severe and life-threatening illness resulting from vitamin B1 (thiamine) deficiency. The prevalence of WE has been estimated from 0.4 to 2.8%. If not treated properly, severe neurologic disorders such as Korsakoff psychosis and even death may occur. The classical triad of clinical symptoms (abnormal mental state, ataxia, and ophthalmoplegia) is found in only 16-33% of patients on initial examination. The originally described underlying condition of WE is alcoholism, but it accounts for about 50% of causes of WE. Nonalcoholic patients are also affected by WE and likely to present symptoms and radiological imaging findings different from patients with alcoholism, which further complicates the diagnosis of WE. Being familiar with predisposing causes, symptoms and radiological imaging findings of WE is important for radiologists and clinicians when making the diagnosis to start immediate treatment. This review discusses pathophysiologies, underlying causes, clinical symptoms, imaging findings and their mimics.

Nutritional Optic Neuropathies: State of the Art and Emerging Evidences

“…Thiamine, or vitamin B1, is a water-soluble B vitamin obtained through the ingestion of whole grains, meat, and fish, and which is absorbed in the gastrointestinal tract and stored in body tissues as thiamine diphosphate. Thiamine diphosphate participates in energy production as an essential cofactor for several enzymes in Krebs cycle, glycolysis, and pentose phosphate pathways [26]. Moreover, vitamin B1 has a role in nucleic acids, neurotransmitters and myelin synthesis, and has an antioxidative effect on nerve cells [8].…”

“…Thiamine deficiency leads to selective neuronal cell death by multiple mechanisms: cellular energy failure, focal lactic acidosis, blood-brain barrier breakdown, mitochondrial dysfunction and oxidative stress [27]. Most common risk factors correlated to thiamine deficiency are alcoholism, unbalanced nutrition, bariatric surgery, hyperthyroidism, and pregnancy [26]. The most frequent manifestation of thiamine deficiency is the Wernicke Korsakoff encephalopathy, which is characterized by the triad: acute confusional state, ataxia, and ophthalmoparesis [28].…”

Wernicke’s encephalopathy — from basic science to clinical practice. Part 1: Understanding the role of thiamine

“…Bariatric surgery, consuming illnesses, malabsorption syndromes, and hyperemesis are other examples of possible causes. 40,41 We will discuss such causes in more detail in the second, forthcoming, part of this review.…”

Wernicke Encephalopathy in an Elderly Patient Due to Chronic Malnutrition From an Atypical Diet

“…Ocular findings can include nystagmus and conjugate gaze palsies due to the involvement of the oculomotor, abducens, and vestibular nuclei. The incidence of WE in the general population is approximately 0.4 to 2.8% compared to 12.5-35.0% in alcohol-dependent individuals [2,3,4]. Overall the prevalence ranges from 1 to 3% worldwide [5].…”

“…Thiamine is vital for aerobic respiration provided by the tricarboxylic acid (TCA) cycle (Figure 2). It is a cofactor for the enzyme pyruvate dehydrogenase which links anaerobic glycolysis to the TCA cycle and as a cofactor for α-ketoglutarate, ultimately produces cellular energy in the form of ATP [3,5]. Notably, with increased dietary carbohydrate intake, the demand for thiamine also increases as it is a key factor in glucose metabolism [8].…”