Wernicke-Korsakoff Syndrome—also called “wet brain”—is a rare but devastating complication of alcohol use disorder. More rarely, a person can develop WKS independent from alcohol use. Epidemiologists estimate 1-2% of Americans suffer from WKS.
There are established treatments for the condition, and clinical researchers are conducting ongoing trials of new treatment options. But, too often, physicians do not diagnose wet brain early enough.
Undiagnosed wet brain is lethal in one out of five patients. Often, late-stage WKS causes irreversible brain damage. It’s critical to identify the syndrome early.
If you are afraid you or a loved one is at risk of developing wet brain, there is hope. Read on to discover the warning signs and symptoms of WKS. Then, learn about the underlying cause of wet brain, and explore the treatment options.
Wet Brain: Critical Signs and Symptoms
Individuals with WKS exhibit recognizable symptoms. Unfortunately, many of these symptoms are similar to those of alcohol intoxication. This similarity is a factor in the under-diagnosis of wet brain among people with alcohol use disorder.
Wet brain symptoms fall into five categories:
- Cognitive symptoms
- Ocular symptoms
- Muscle and motor symptoms
- Mood, sensory, and perception symptoms
- Physiological regulation dysfunction
You will note different symptoms at different stages of the disease. Look out for the following warning signs.
Cognitive Symptoms of Wet Brain
The cognitive symptoms of wet brain impact memory and problem-solving. In the later stages of WKS, patients may not be able to form new memories or learn new information. Even in the earliest stages, people with WKS often exhibit the following cognitive symptoms:
- Distorted memory
- Confusion and disorientation
- Loss of ability to follow directions
Wet brain can disrupt all parts of memory: encoding, storage, and retrieval. At the end stages, a patient may have a socially normal conversation but forget the conversation an hour later. Acute executive process dysfunction is typically a sign WKS has progressed to a later stage.
Ocular Symptoms of Wet Brain
The telltale signs of WKS are eye-related symptoms. Most noticeable is nystagmus, the medical term for repetitive, uncontrollable eye movements.
Nystagmus reduces depth perception and clarity of vision. It also impacts balance. Other ocular symptoms include:
- Conjugate gaze palsies
- Pupillary sluggishness
These symptoms are the result of ocular nerves that have become dysfunctional or paralyzed. Conjugate gaze palsies limit the direction of eye movement. Anisocoria means “different-sized pupils.”
Ptosis describes an upper eyelid that droops over the eye. Pupillary sluggishness is when the pupil has a slow, delayed reaction to changes in light.
Muscle and Motor Symptoms of WKS
The most common muscle and motor symptoms of wet brain are gait ataxia, weakness, and fatigue. Ataxia is poor coordination of muscle movements. Gait ataxia is a problem coordinating the muscles necessary to walk.
For some, gait ataxia becomes so severe the patient can no longer walk.
Fatigue and weakness are tiredness. It often manifests as weakness in the limbs. The earliest stages of WKS can also cause delirium tremens, or “the shakes.”
Mood, Sensory, and Perception Symptoms
WKS can cause hallucinatory symptoms. It can also alter someone’s sense of smell. The most common mood, sensory, and perception symptoms are:
- Visual and auditory hallucinations
- Distorted perception of time
- Mental disturbances
- Distal sensory loss
Distal sensory loss is the loss of the sense of touch in hands or feet. This can present as numbness or intermittent pain. This loss occurs when WKS causes peripheral neuropathy.
Physiological Regulation Dysfunction
Ultimately, wet brain is lethal when the body can no longer maintain homeostasis due to the disease. As the disease progresses, a WKS patient may fall into a coma. Before that, physicians may observe the following dysfunctions of regulation:
- Low blood pressure
An acute drop in blood pressure often precipitates a coma.
What Causes Wet Brain?
At root, Wernicke-Korsakoff Syndrome is an effect of thiamine deficiency. Thiamine is a vitamin. Nutritionists call thiamine “vitamin B1.”
In high-income, industrialized nations, like the United States, most people get enough vitamin B1 in their diet. Foods as diverse as pork, yogurt, peas, and enriched cereals include plenty of thiamine.
So, most thiamine deficiencies develop when the body cannot absorb the nutrients from food properly. People with conditions that impact digestive organs are at high risk for thiamine deficiency. This can include:
- Celiac disease
- Crohn’s disease
- Pancreatic failure
- Ulcerative colitis
- Bariatric surgery
- Alcohol use disorder
However, B1 deficiency doesn’t automatically become WKS. Instead, WKS is brain and nerve cell damage that results from prolonged thiamine deficiency. It progresses from Wernicke encephalopathy to Korsakoff Syndrome.
Alcohol Use Disorder and WKS
Long-term heavy drinking is the key sign of alcohol use disorder. Alcohol use disorder puts people at high risk for thiamine deficiency. Approximately 80% of people with alcohol addiction develop vitamin B1 deficiency.
Alcohol use disorder inflames the lining of the stomach and digestive tract. This hampers the digestive system’s ability to pull necessary vitamins and proteins from food. Stomach and digestive tract inflammation can cause malnutrition more broadly.
Thiamine is a cofactor. That is, it’s a chemical compound that empowers enzymes to trigger biochemical reactions. In the human digestive system, thiamine helps enzymes run through the biochemical process that turns carbohydrates into energy.
This process is also critical to use the nutrients and proteins in food. The nutrients and proteins pulled from food become the building blocks of nervous-system cells and muscle tissue. They’re also passed through other physiological systems that, ultimately, transform the nutrients into vital neurochemicals.
Neurochemical exchange is the foundation of mental processes.
Thiamine is so foundational to digesting and using food, its absence causes disastrous effects quickly. It also accelerates quickly. As low thiamine levels inhibit digestive enzymes, those enzymes are less able to pull thiamine from food.
This creates a dangerous downward spiral of malnutrition.
Cellular Damage (Wernicke Encephalopathy)
Wernicke encephalopathy begins when a body can no longer replenish nerve cells and muscle cells. Due to the vitamin B1 deficiency, digestive enzymes cannot draw necessary nutrients from food to make new cells.
Nerve cells and muscle cells become damaged and dysfunctional. This, in turn, causes the primary symptoms of WKS: impaired coordination, abnormal eye movements (or eyeball paralysis), and disorientation.
Eventually, cellular disrepair damages the brain’s thalamus and hypothalamus. These structures are responsible for much of the body’s homeostasis. Damage to these parts of the brain disrupts homeostasis, which can cause:
- Low blood pressure
These symptoms are acute. Often, they’re lethal.
Korsakoff Psychosis Syndrome
If Wernicke’s encephalopathy goes untreated, the damage induces Korsakoff psychosis. Korsakoff psychosis is a neuropsychological disorder. It causes acute memory loss and problems learning new information.
Korsokoff is characterized by changes in mood, behavior, and memory. It also causes disorientation and hallucinations.
Symptoms can persist for a few days or several weeks. Once Korsakoff has set in, it cannot be reversed.
Stages of Wernicke-Korsakoff Syndrome Progression
WKS progresses through distinct recognizable stages. But, many patients do not exhibit all symptoms at each stage. As a result, the earliest stages of WKS are underdiagnosed.
There are two well-defined stages of WKS: Wernicke encephalopathy and Korsakoff psychosis. Wernicke encephalopathy is acute, while Korsakoff psychosis is long-term.
WKS is progressive because thiamine deficiency harms digestive enzymes. As enzymes have less and less capacity to use the nutrients in food—including thiamine—the thiamine deficiency worsens.
Alcohol neurotoxicity can speed up the progression of the disease. Alcohol neurotoxicity has a direct, harmful effect on nerve cells. The double-impact of alcohol neurotoxicity and thiamine deficiency increases the rate of decline.
Supplemental thiamine treatments cannot reverse the damage done by alcohol neurotoxicity.
WKS Diagnosis, Treatment Options
In its early stages, clinicians can treat Wernicke-Korsakoff Syndrome with intravenous thiamine and glucose. Sometimes, physicians prescribe oral vitamin B1 supplements. Patients may meet with a nutritionist, who can determine the appropriate dietary changes.
Thiamine deficiencies are typically one facet of general malnourishment. If WKS is caused by alcohol use disorder, the nutritionist will recommend a safe path to alcohol cessation. To switch to an alcohol-free diet safely, patients must be under medical care to mitigate the risks of alcohol withdrawal.
Patients must be sober during the diagnostic process.
When a patient presents symptoms that suggest they may have WKS, clinicians should begin the diagnostic process. This process determines whether a patient has Wernicke-Korsakoff Syndrome or a different disorder with similar symptoms. Diagnostic tests may rule out:
- Hepatic encephalopathy
- Chronic hypoxia
- Normal-pressure hydrocephalus
- Alcohol withdrawal syndrome
Patients with alcohol withdrawal syndrome have similar symptoms to those with WKS. But, alcohol withdrawal syndrome typically only lasts up to four days. Moreover, it does not impact a patient’s metabolic process or hypothalamus signaling.
Thus, clinicians diagnose WKS by examining those factors.
Diagnosis calls for a complete metabolic panel. This series of blood tests determine the levels of different proteins and hormones in the blood, which can indicate thiamine deficiency. The American Medical Association recommends measuring a patient’s Erythrocyte transketolase levels to diagnose Wernicke encephalopathy.
Complete Neurological Exam
A neurological exam will include cerebellar function testing. These tests rate motor coordination. Some clinical manuals call these tests the “cerebellar motor exam.”
Neurological exams can include MRI or CT tests. These tests can reveal the following signs of WKS in the brain:
- Visible signaling hyperintensities
- Symmetrical lesions in different brain regions
- Volume loss (specifically shrunken brainstem nuclei)
Hyperintensities are bright white spots visible in an MRI image. This indicates damage to white matter and subcortical nuclei. These tests can substantiate a WKS diagnosis.
Personal and Family History
Clinicians will explore the patient’s medical history. They will also examine the medical history of the patient’s family.
Studies show people can be genetically predisposed to vitamin B1 deficiency. So, if a patient’s family members have a history of deficiency, a WKS diagnosis is more likely.
Clinicians will take into account a patient’s medical history to, likewise, determine the likelihood that WKS is the source of their symptoms. A history of an alcohol use disorder, anorexia, or bariatric surgery makes WKS more likely.
Wet brain treatment varies. Medical experts emphasize the importance of immediate treatment with IV thiamine and glucose supplements. Oral supplements are not as effective.
It is better to err on the side of too high a dosage of supplemental B1 than too little. Physicians may also prescribe supplemental magnesium and other vitamins to treat comorbid deficiencies. It is also critical to treat any underlying causes of WKS.
Korsakoff Syndrome Treatment
Supplemental thiamine is not enough to treat late-stage wet brain on its own. A patient experiencing Korsakoff syndrome requires more extensive, integrated care.
Medical teams typically recommend brain injury rehabilitation therapy, residential support, and cognitive-behavioral therapy.
Korsakoff treatment also requires carers to establish a routine for the patient. This can mitigate the effect of amnesia.
Most patients with Korsakoff psychosis will not recover enough neurological function to live independently. Ultimately, Korsakoff psychosis instigates irreversible confusion.
Treatment Options Under Development
Medical scientists are currently studying phenytoin as a treatment for WKS. Phenytoin has restored memory function in animal studies. Ongoing trials also seek to determine the optimal thiamine dosage to treat WKS.
Can You Prevent Wet Brain?
For many people, it’s possible to prevent wet brain before it develops. To prevent WKS, you must address the underlying causes before it develops. This means treating alcohol use disorder or anorexia.
Clinicians can also prevent wet brain. If a patient suffers from alcohol addiction or anorexia, clinicians can administer thiamine supplements pre-emptively. This can prevent cellular damage before it occurs.
Preventative intravenous thiamine injections are sometimes prescribed for patients recovering from bariatric surgery.
Friends and family can help prevent wet brain by encouraging at-risk individuals to seek treatment before it develops.
Alcohol Use Disorder Treatment: Get Help Now
If you’re struggling with alcohol use disorder, you are not alone. Treatment is available today.
Maybe you’re already struggling with the effects of wet brain. Or, maybe you believe your alcohol use has negatively impacted your quality of life.
If you’re ready to get help, contact us. We’ll help you find a provider near you.