OVERVIEW

What is Wernicke encephalopathy?

Wernicke encephalopathy (WE), also known as Wernicke's encephalopathy, is a complication caused by thiamine (vitamin B₁) deficiency and represents one stage of Wernicke-Korsakoff syndrome. It is a neurological emergency.

The disease is primarily characterized by symptoms such as double vision, impaired eye movement, mental abnormalities, and unsteady gait. Early and timely treatment can significantly improve symptoms and prognosis.

Is Wernicke encephalopathy common?

It is relatively common, with an annual incidence rate of approximately 6.5 per 100,000 people. Middle-aged men, particularly those with alcohol abuse, are more frequently affected.

SYMPTOMS

What are the symptoms and manifestations of Wernicke's encephalopathy?

Patients with Wernicke's encephalopathy primarily present with the triad of sudden-onset ophthalmoplegia, mental abnormalities (encephalopathy), and gait ataxia, though this triad does not appear in all cases.

However, in individuals with alcoholism, the presence of this triad can directly lead to a diagnosis of WE.

• Ophthalmoplegia may manifest as double vision, dizziness, blurred vision, ptosis, etc. Bilateral abducens nerve palsy is common, and nystagmus, papilledema, or retinal hemorrhage may also occur. Eye movement disorders typically do not appear in isolation but rather as part of a combined presentation.
• Mental abnormalities (encephalopathy) may include poor concentration, significant memory decline, disorientation, wandering, as well as distractibility, irritability, apathy, and dementia. These symptoms can sometimes be difficult to distinguish from alcohol withdrawal and may also involve confusion, lethargy, or coma.
• Ataxia may present as unsteadiness while standing or walking, with severe cases possibly being unable to walk. However, upper limb movement is generally less affected.
• Others: In addition to the classic triad, most patients also exhibit hypothermia, hypotension, and tachycardia. Some may have comorbidities such as liver disease, heart failure, pancreatitis, or peripheral neuropathy, which are common in chronic alcoholism.

What conditions should Wernicke's encephalopathy be differentiated from?

This disease must be distinguished from other brain disorders that cause ophthalmoplegia, mental and behavioral abnormalities, and ataxia, such as top-of-the-basilar artery stroke, hypoxic-ischemic encephalopathy after cardiac arrest, herpes simplex encephalitis, and third ventricle tumors.

It should also be differentiated from other conditions related to chronic alcoholism, such as chronic alcoholic encephalopathy.

CAUSES

What is the cause of Wernicke's encephalopathy?

The cause of Wernicke's encephalopathy is thiamine (vitamin B₁) deficiency. Thiamine is primarily obtained through diet:

• Alcoholics often replace meals with alcohol, sometimes going days without eating, leading to insufficient thiamine intake;
• Chronic alcohol abuse causes gastrointestinal dysfunction and small intestinal mucosal damage, resulting in malabsorption, which further exacerbates thiamine deficiency;
• Alcoholism increases the incidence of chronic liver disease, reducing the body's ability to store and convert thiamine.

Insufficient thiamine and its metabolites can impair glucose metabolism, leading to lactic acid accumulation and acidosis in brain tissue, disrupting the synthesis, release, and uptake of neurotransmitters, and ultimately causing central nervous system dysfunction and Wernicke's encephalopathy.

If Wernicke's encephalopathy is caused by thiamine deficiency, what are the causes of thiamine deficiency?

Thiamine deficiency has many causes, including severe and prolonged vomiting in pregnant women, malnutrition, anorexia nervosa, liver disease, gastrointestinal disorders or surgical history, malignant tumors, pernicious anemia, chronic diarrhea, long-term renal dialysis, prolonged parenteral nutrition lacking thiamine, long-term fluid replacement, and magnesium deficiency.

All of these conditions that can lead to thiamine deficiency may also trigger the onset of Wernicke's encephalopathy.

DIAGNOSIS

How is Wernicke's encephalopathy diagnosed?

The diagnosis of Wernicke's encephalopathy (WE) is primarily based on the patient's history of chronic alcoholism or malnutrition, clinical manifestations, and typical findings on brain MRI. In patients with chronic alcohol abuse, WE can be diagnosed if they meet 2 of the following 4 Caine criteria:

• Dietary deficiency;
• Oculomotor abnormalities;
• Cerebellar dysfunction (e.g., ataxia);
• Altered mental status or mild memory impairment.

What tests are needed for patients with Wernicke's encephalopathy? Why are these tests performed?

• Brain CT or MRI: WE may present with characteristic bilateral thalamic and periaqueductal brainstem lesions, as well as mammillary body atrophy. CT or MRI imaging helps confirm the diagnosis and rule out other conditions, with MRI being more sensitive for early detection.
• B-vitamin testing: Since WE is caused by vitamin B₁ deficiency, measuring vitamin B₁ levels can aid diagnosis. However, blood B-vitamin levels do not fully reflect brain levels, so normal blood vitamin B₁ does not exclude WE.
• Liver function tests, liver ultrasound, and cardiac evaluation: These assess organ damage related to chronic alcoholism.

What precautions should patients with Wernicke's encephalopathy take during an MRI scan?

Magnetic resonance imaging (MRI) offers high resolution for central nervous system evaluation, aiding clinical diagnosis and treatment. Before the scan, patients must ensure they have no metal objects in their body (including dentures, implants, surgical screws/plates, etc.) and remove external metal items like phones, keys, glasses, and belts. During the scan, patients must lie flat inside the MRI machine.

The procedure involves some noise, and the enclosed space may cause discomfort for those with claustrophobia. Scan duration varies by sequence, typically ranging from several minutes to tens of minutes.

No special precautions are needed post-scan, though increased water intake is recommended after contrast-enhanced MRI to aid excretion.

TREATMENT

Which department should I visit for Wernicke's encephalopathy?

Neurology.

Can Wernicke's encephalopathy heal on its own?

No. This disease is actually an emergency condition. Without early and timely treatment, it may progress to coma or even become life-threatening.

Does Wernicke's encephalopathy require hospitalization?

Yes.

How is Wernicke's encephalopathy treated?

Diagnosing Wernicke's encephalopathy is relatively difficult. When clinical suspicion arises, treatment should begin immediately without delay for further testing.

For patients suspected of having WE, parenteral thiamine should be administered immediately. This approach is currently considered safe, effective, and relatively inexpensive.

Specific treatment protocol: Administer 500 mg of thiamine intravenously over 30 minutes, three times daily for 2 days; followed by 250 mg of thiamine intravenously or intramuscularly once daily for 5 days, along with other B vitamins.

Note: Administering glucose without thiamine may trigger or worsen WE. Therefore, thiamine should always be given before glucose.

If patients remain at risk after the above treatment, oral thiamine and multivitamin supplements may be continued.

Can Wernicke's encephalopathy be cured with timely treatment? What is the typical prognosis?

Rapid thiamine administration can improve ocular signs within hours to days. If ocular paralysis shows no response to treatment, alternative diagnoses should be considered.

Ataxia and vestibular function typically improve after about 2 weeks of treatment. Generally, the prognosis is fair, though some patients may experience residual symptoms such as nystagmus or gait instability.

DIET & LIFESTYLE

What should Wernicke's encephalopathy patients pay attention to in their diet?

For patients with Wernicke's encephalopathy caused by chronic alcoholism, the first step is to abstain from alcohol. Additionally, they should focus on nutritional intake, consuming more fruits and vegetables rich in vitamins.

What should Wernicke's encephalopathy patients pay attention to in daily life?

Due to blurred vision and unsteady gait, Wernicke's encephalopathy patients are prone to falls, requiring close supervision by caregivers. Some patients may exhibit significant psychiatric symptoms such as agitation or irritability, necessitating increased care to prevent self-harm or harm to others. In severe cases, patients may become comatose or bedridden, requiring regular repositioning and back patting to prevent bedsores, deep vein thrombosis, or hypostatic pneumonia.

Most Wernicke's encephalopathy patients are chronic alcoholics, making alcohol abstinence crucial (while remaining vigilant for withdrawal syndrome symptoms).

Does Wernicke's encephalopathy require follow-up examinations? How is it monitored?

Yes, follow-up is necessary. Typically, symptom progression is observed, and brain MRI scans are repeated.

Can Wernicke's encephalopathy patients fly, engage in strenuous exercise, or travel to high-altitude areas?

It is not recommended before the disease is effectively treated.

PREVENTION

Can Wernicke's encephalopathy be prevented?

• Most cases of Wernicke's encephalopathy are caused by vitamin deficiencies resulting from chronic alcoholism. Therefore, avoiding long-term heavy alcohol consumption is the primary way to prevent the disease.
• Secondly, maintaining a healthy and balanced daily diet ensures adequate vitamin intake.
• For Wernicke's encephalopathy secondary to other diseases (such as gastrointestinal disorders), malabsorption due to underlying conditions can also lead to vitamin deficiencies. Thus, such patients should regularly receive vitamin B₁ supplementation via intramuscular or intravenous injections to prevent the disease.
• In patients not suspected of having thiamine deficiency, WE may be iatrogenically induced by glucose administration. To avoid this complication, administering thiamine before or simultaneously with glucose infusion has become standard practice in emergency departments, especially for patients at risk of thiamine deficiency.