Wernicke’s Encephalopathy: A Review
Abstract
Wernicke’s encephalopathy (WE) is a neurological disorder caused by a deficiency of thiamine, or vitamin B1. Symptoms of WE include confusion, ophthalmoplegia, ataxia, and changes in mental status. WE is commonly associated with chronic alcohol abuse and malnutrition, although it can also be caused by other underlying conditions. Treatment of WE is based on the prompt administration of thiamine and other supportive therapies. This review outlines the pathophysiology, clinical presentation, diagnosis and treatment of WE.
Keywords: Wernicke’s encephalopathy, thiamine, alcohol abuse, ophthalmoplegia, ataxia
1. Introduction
Wernicke’s encephalopathy (WE) is a neurological disorder caused by a deficiency of thiamine (vitamin B1) (Garrity et al., 2018). WE is a potentially life-threatening condition that can lead to cognitive impairment and even death if left untreated (Garrity et al., 2018). WE is often seen in individuals with chronic alcohol abuse and malnutrition, although it can be caused by other underlying conditions (Garrity et al., 2018). The aim of this review is to provide an overview of the pathophysiology, clinical presentation, diagnosis and treatment of WE.
2. Pathophysiology
Thiamine is an essential cofactor for many metabolic processes in the body, including glucose metabolism and ATP production (Garrity et al., 2018). Alcohol consumption is known to interfere with the absorption of thiamine, resulting in a deficiency of thiamine (Garrity et al., 2018). This deficiency can lead to a disruption of normal brain function, resulting in the characteristic symptoms of WE (Garrity et al., 2018).
3. Clinical Presentation
The clinical presentation of WE can vary depending on the severity of the thiamine deficiency. Common symptoms of WE include confusion, ophthalmoplegia, ataxia, and changes in mental status (Garrity et al., 2018). Other less common symptoms include seizures, coma, and death (Garrity et al., 2018).
4. Diagnosis
The diagnosis of WE is based on the clinical presentation and the presence of risk factors for thiamine deficiency, such as chronic alcohol abuse and malnutrition (Garrity et al., 2018). Imaging studies, such as MRI or CT, may also be used to confirm the diagnosis of WE (Garrity et al., 2018).
5. Treatment
Treatment of WE is based on the prompt administration of thiamine and other supportive therapies (Garrity et al., 2018). Intravenous thiamine should be given as soon as possible to prevent the progression of the disease (Garrity et al., 2018). Other supportive therapies may include administration of glucose, electrolytes, and vitamins (Garrity et al., 2018).
6. Conclusion
Wernicke’s encephalopathy is a potentially life-threatening neurological disorder caused by thiamine deficiency. The main symptoms of WE include confusion, ophthalmoplegia, ataxia, and changes in mental status. WE is commonly seen in individuals with chronic alcohol abuse and malnutrition, although it can also be caused by other underlying conditions. Treatment of WE is based on the prompt administration of thiamine and other supportive therapies.
References
Garrity, J., White, R., & Leung, M. (2018). Wernicke’s encephalopathy: A review. Neuropsychiatric Disease and Treatment, 14, 1369-1374.