wernicke encephalopathy

What is Wernicke Encephalopathy?

Our brains rely on various minerals, vitamins, and fatty acids to function normally. Deficits of one or more of these substances prevent the brain from functioning as it should. According to the National Institute of Neurological Disorders and Stroke, Wernicke encephalopathy (WE) is a degenerative disorder affecting the brain. It usually arises from a deficiency in thiamine, a vitamin also known as B1.

To function properly, the brain needs a constant and efficient source of thiamine. Insufficient thiamine levels may impair glucose metabolism in the brain and cause mitochondrial dysfunction.

Mitochondria are substances in our body’s cells that produce adenosine triphosphate (ATP) when glucose is being metabolized. Dysfunctions in mitochondria deplete our body’s ATP levels and increase the number of unpaired electrons known as free radicals. These conditions may injure neural elements such as the blood-brain barrier and myelin sheaths and may reduce the number of neurotransmitters. Such damages contribute to the onset of Wernicke encephalopathy symptoms.

Wernicke encephalopathy is a neurological emergency that should be treated as soon as possible. If left untreated, it may progress to an irreversible stage known as Wernicke Korsakoff syndrome, a condition sometimes known as wet brain. People with Wernicke encephalopathy have varied neurocognitive manifestations usually involving changes in mental status as well as oculomotor dysfunction and gait (problems with the eye muscles and movement).

Often, the disorder develops because of alcohol use disorder (AUD). The diagnosis of WE is clinical. Doctors usually conduct a differential diagnosis to rule out the possibility of other conditions with similar symptoms. Laboratory tests may confirm thiamine deficiency, and when a case is ambiguous, medical professionals perform brain imaging to help with diagnosis.

Data from the National Survey on Drug Use and Health (NSDUH) reported that about 15.1 million adults ages 18 and above had alcohol use disorder (AUD) in 2015. Only about 6.7 percent of individuals in this age group who had alcohol use disorder in the previous year sought treatment. The 15 million Americans struggling with alcohol use disorder are at risk of developing Wernicke encephalopathy since this condition is frequently associated with the abuse of alcohol.

The Causes of Wernicke Encephalopathy

Inadequate supply of vitamin B1 or thiamine to an individual’s brain is considered the underlying cause of the disorder. Thiamine deficiency may occur due to poor nutrition, various medical conditions, or the inability of the intestines to absorb vitamin B1. Starvation, hemodialysis-induced thiamine deficiency among patients with the last phase of the renal disease, and thiamine deficient formulas are other issues associated with thiamine deficiency.

Misuse of alcohol can also cause Wernicke encephalopathy. Chronic alcohol misuse is a common cause of the disorder. About 30 to 80 percent of individuals who abuse alcohol have thiamine levels that are below normal. Chronic alcohol abusers tend to have a higher propensity of developing Wernicke encephalopathy because:

  • Alcohol and malnutrition work singly or together to reduce the absorption of thiamine.

  • Their level of self-care and adherence to healthy diets are poor.

  • The hepatic (liver-related) storage of vitamin B1 or thiamine is low.

  • The neurotoxicity of ethanol (alcohol) impairs how the body uses thiamine.

  • They have increased demand for thiamine because it is increasingly used to metabolize alcohol.

Signs and Symptoms of Wernicke Encephalopathy

Wernicke encephalopathy has high mortality and morbidity rates. In about 80 percent of the time, professionals do not diagnose the condition until autopsy procedures. Without diagnoses, people may receive little to no treatment and experience irreversible brain damage.

Individuals with thiamine deficiency may show signs and symptoms such as nausea, vomiting, loss of appetite, memory loss, giddiness, weakness, fatigue, apathy, diplopia (double vision), anxiety, insomnia, and concentration difficulties. These are the early signs of a thiamine deficiency.

People who have histories of abusing alcohol and who display the following symptoms should be examined and tested for WE:

  • Confusion (the most common sign in people with the disorder)

  • Oculomotor dysfunction (problems with the muscles that control the eyes)

  • Gait ataxia (problems with coordination)

Oculomotor abnormalities, confusion, and dysfunction or ataxia related to the cerebellum and coordination are jointly regarded as the classic triad. The presence of such symptoms is often a diagnostic indicator of Wernicke encephalopathy.

Because most patients will not exhibit all three signs at the same time, it that may result in the underdiagnosis of WE. Such underdiagnosis could be dangerous, as the consequences of inadequate treatment of the condition are significant.

Oculomotor dysfunction may produce vision problems such as gaze-induced horizontal and vertical nystagmus. Nystagmus is a condition that produces repetitive, uncontrolled eye movements. Oculomotor dysfunction may also produce other symptoms, such as double vision, also known as diplopia.

A person with oculomotor dysfunction may also experience conjugate gaze palsy, a neurological disorder in which an individual is unable to move his or her eyes in the same direction. Another symptom of WE is ataxic gait, which is often characterized by unsteady staggering, a type of walking that is uncoordinated and not ordered.

Only about one-third of people with WE experience the classical triad of symptoms. On the onset of WE, it may be subacute, acute, or chronic. People who experience confusion may be apathetic, have impaired awareness of immediate situations, and lack the ability to concentrate.

Sadly, comas are another way to recognize Wernicke encephalopathy. For some people, it may be the sole manifestation of the condition. Others may experience a loss of equilibrium during the early stages of the condition. For others, dysfunction in the areas of the brain known as the cerebellum may cause gait ataxia in the chronic and subacute stages.

Other symptoms associated with Wernicke encephalopathy are:

  • Cardiovascular dysfunction, including exertional dyspnea and tachycardia (breathing difficulties and rapid heartbeat)

  • Peripheral neuropathy characterized by foot drop, paresthesia, and reduced deep tendon reflexes (nervous disorders that affect different areas of the body)

  • Autonomic dysfunction that presents in the form of hypotension, hypothermia, or syncope (problems in the autonomic nervous system that may cause low blood pressure, low body temperature, or fainting)

  • Memory disturbances

  • Delirium

Treatment and Management of Wernicke Encephalopathy

Treatment of Wernicke encephalopathy involves introducing vitamin B1 or thiamine and proper hydration and nutrition. People with the condition typically need high-dose intravenous thiamine (IV) therapy along with long-term supplementation of thiamine. Individuals who consume alcohol should stop drinking it.

Stopping the use of alcohol can help prevent further brain damage and other deterioration. Without treatment, WE can be life-threatening. If you misuse alcohol or are addicted to it, seek professional help. Rehab facilities and treatment programs may help you recover from alcohol abuse and stop the progression of the condition.