Wernicke-Korsakoff syndrome (WKS) is a severe brain disorder usually linked to chronic heavy alcohol use and a deficiency of vitamin B1 (thiamine). [1] It comprises two related conditions – an acute episode of Wernicke’s encephalopathy followed by Korsakoff’s syndrome (a chronic memory disorder) if the first phase is left untreated. [1] Without early intervention and prompt treatment, WKS can cause permanent brain damage, memory loss, or even death.
- Wernicke-Korsakoff syndrome results from a severe thiamine (vitamin B1) deficiency, most commonly due to long-term alcohol misuse.
- It involves an acute Wernicke’s encephalopathy (sudden brain dysfunction with confusion and coordination problems) that can progress to Korsakoff’s syndrome (a chronic memory disorder) if not treated.
- Prompt thiamine treatment can reverse early Wernicke’s encephalopathy, but once Korsakoff’s syndrome develops, the resulting memory loss is often irreversible.

Understanding Wernicke-Korsakoff syndrome
Wernicke-Korsakoff syndrome refers to a spectrum of two related neuropsychiatric conditions caused by thiamine deficiency. The first is Wernicke’s encephalopathy, followed by Korsakoff’s syndrome if the acute phase is not effectively treated.
What is Wernicke's encephalopathy?
Wernicke’s encephalopathy is an acute neurological syndrome caused by severe thiamine deficiency. It is a medical emergency characterized by mental confusion, difficulty with muscle coordination (ataxia), and abnormal eye movements such as nystagmus (rapid eye oscillation) or double vision. [2][3] If recognized early and treated with high-dose thiamine, Wernicke’s encephalopathy can often be reversed, preventing progression to the chronic stage. [1][2]
What is Korsakoff syndrome?
Korsakoff syndrome (Korsakoff’s psychosis) is the chronic phase of WKS that typically follows unresolved Wernicke’s encephalopathy. It is essentially a permanent memory disorder resulting from irreversible brain damage due to prolonged thiamine deficiency. [1]
People with Korsakoff’s have severe difficulty forming new memories and often confabulate (unknowingly fill in memory gaps with fabricated information). [4] Other features include apathy and sometimes hallucinations. [1] Unlike Wernicke’s, Korsakoff’s syndrome is not immediately life-threatening, but its cognitive effects are usually long-lasting and can dramatically impair independent living.
Symptoms
The signs and symptoms of WKS reflect its two-phase progression from an acute neurologic state to a chronic cognitive disorder:
Wernicke’s encephalopathy (acute phase)
- Marked confusion and disorientation
- Loss of muscle coordination (ataxia), causing a staggering or wide-based gait
- Abnormal eye movements (nystagmus, double vision) ± partial ophthalmoplegia
- Obvious malnutrition: significant weight loss, muscle-wasting limbs, gaunt facial appearance
- Tremor or coarse limb jerks; occasional postural hypotension or hypothermia
- Can deepen to stupor or coma if thiamine treatment is delayed [1]
Korsakoff syndrome (chronic phase)
- Severe memory loss and inability to form new memories
- Frequent confabulation to fill memory gaps
- Apathy and lack of insight into the cognitive deficit
- Repetitive questions or behaviors (perseveration)
- Occasional hallucinations or mild delusions
- Ongoing signs of poor nutrition, such as low body weight or nerve damage from vitamin deficiencies [1]
Without treatment, the acute Wernicke’s signs will typically give way to the chronic Korsakoff symptoms described above as the brain damage progresses.
Causes of Wernicke-Korsakoff syndrome
As mentioned, WKS is caused by severe thiamine deficiency. Thiamine is a coenzyme for brain enzymes that convert glucose into compounds the cell can use in its energy cycle. Without it, those pathways collapse, and neurons quickly become energy-starved and start to degenerate. [5] The most common reason for severe thiamine deficiency is chronic heavy alcohol use, since alcohol leads to poor nutrition and impairs thiamine absorption. [1]
Is it always related to alcohol use?
Alcohol misuse is the leading cause of WKS, but it is not the only cause. Any condition that results in severe malnutrition or vitamin B1 deficiency can potentially trigger Wernicke-Korsakoff syndrome. [3] In rare cases, people who do not drink heavily can develop WKS due to other factors that deplete thiamine.
For example, prolonged starvation or vomiting (e.g., from an eating disorder or severe morning sickness), advanced cancers, AIDS, or certain gastrointestinal surgeries (such as bariatric weight-loss surgery) that cause malabsorption. [1]Â However, these non-alcohol causes are far less common than alcohol-related cases. [1]
Is it fatal?
Wernicke-Korsakoff syndrome can be life-threatening if not treated promptly. Wernicke’s encephalopathy is a medical emergency. If left untreated, it is estimated to be fatal in up to 20% of cases. [6] Even when not immediately deadly, unchecked WKS can cause irreversible brain damage and significantly shorten lifespan. The encouraging news is that with timely thiamine treatment, many patients survive the acute phase of Wernicke’s encephalopathy and avoid the worst outcomes. [1]
Diagnosing Wernicke-Korsakoff syndrome
Doctors diagnose Wernicke-Korsakoff syndrome by recognizing a pattern. It’s not about waiting for a blood test or scan—doctors spot signs early enough to start thiamine before the brain is permanently damaged.
The context mattersÂ
During the initial assessment, doctors take a history and look for clear risk factors that deplete vitamin B1: [1]Â
- Long-term heavy alcohol use
- Recent severe weight loss or malnutrition (dietary deficiencies)
- Prolonged vomiting (more than 2 weeks)
- Recent bariatric surgery
- Chronic dialysis, advanced HIV/AIDS, or metastatic cancer
Simultaneously, they check for key signs of Wernicke’s encephalopathy.Â
These include: [1]Â
- Eye movement problems (nystagmus, gaze palsy, or difficulty tracking objects)
- An unsteady or wide-based walk (ataxia)
- Confusion, disorientation, or sudden apathy
The presence of two of these signs in someone at risk is sufficient to diagnose acute Wernicke’s encephalopathy and emphasizes the need to initiate immediate treatment. They must also rule out acute intoxication, as the same symptoms may be present. [7]
The patient’s memory is screened during the same visit.
Severe short-term memory loss, especially when filled with inaccurate or invented stories (confabulation), indicates that the chronic Korsakoff stage has already started. [3]Â
Imaging and labs may follow, but treatment shouldn’t be delayed.Â
Doctors may order an MRI to look for changes in the mammillary bodies or thalamus, or check thiamine levels in the blood. But treatment begins immediately—there’s no benefit in waiting for results. [8]Â
If memory problems persist after the acute illness settles, the diagnosis of Korsakoff syndrome is confirmed. Together, these findings form the complete clinical picture of Wernicke-Korsakoff syndrome.
Treatment for Wernicke-Korsakoff syndrome
WKS treatment occurs in two stages: first, addressing the immediate, acute symptoms (Wernicke’s encephalopathy), and then managing chronic, persistent memory impairment (Korsakoff syndrome).
Stage 1: Acute phase – Wernicke’s encephalopathyÂ
- Administer thiamine first. Start IV/IM thiamine immediately before any glucose-containing fluids or high-carb foods to avoid causing brain injury. [9]Â
- Simultaneously correct magnesium and electrolytes. Magnesium is the co-factor that allows thiamine to convert into its active form; without it, thiamine therapy becomes ineffective. [10]Â
- Feed cautiously once thiamine is being administered. Begin balanced nutrition only after the initial thiamine dose, then increase calorie intake gradually while monitoring phosphate, potassium, and magnesium levels to prevent refeeding syndrome. [10]
Stage 2: Chronic phase – Korsakoff syndrome (KS)
- Stay on oral thiamine long-term. After the IV course, daily oral thiamine continues for weeks and often indefinitely, because body stores remain fragile. [1]
- Maintain complete abstinence from alcohol. Detox and structured rehabilitation are essential; continued drinking accelerates neurodegeneration and hinders recovery. [9]
- Introduce cognitive processes rehabilitation. Techniques such as errorless learning, external memory aids, set routines, and (when needed) supervised living can help people regain everyday skills despite significant amnesia. [9]
Can it be reversed?
Wernicke encephalopathy (acute phase) can often be fully reversed if thiamine therapy starts promptly, significantly improving symptoms such as confusion, coordination issues, and eye abnormalities. [1]
However, Korsakoff syndrome (chronic phase) typically leads to lasting memory deficits and cognitive impairments. Only about 25% of patients achieve substantial recovery. Around half improve somewhat but live with lasting memory problems, while the remaining group face permanent, severe impairment, often needing lifelong support. This frequently includes supported housing, structured supervision, or long-term care facilities for those with significant memory loss.[6]
Final thought
WKS is largely preventable and is a testament to the severe brain damage that can result from chronic alcohol abuse. Maintaining good nutrition and avoiding excessive alcohol are key to prevention. For those at risk, recognizing the early signs of Wernicke’s encephalopathy and getting immediate thiamine treatment can halt the progression to Korsakoff’s.
If left unchecked, WKS can cause permanent memory loss and cognitive decline that significantly affect quality of life. Ultimately, preventing WKS through healthy habits is far better than trying to treat it after brain damage has occurred.