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September 8, 2018

What is “Wet Brain” or Wernicke-Korsakoff Syndrome?

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What is wet brain?Wet brain,” officially known as “Wernicke-Korsakoff Syndrome” (WKS), is a serious neurological disorder caused by habitual, long-term alcohol abuse. The disorder was named after Russian physician Sergei Korsakoff and German scientist Carl Wernicke, who pioneered the clinical experimentation and conducted the research leading to its founding.

Wet brain actually consists of two separate, co-occurring disorders: Wernicke’s encephalopathy and Korsakoff’s psychosis. Wernicke’s encephalopathy describes the acute neurological symptoms resulting from biochemical lesions throughout the central nervous system (CNS). Korsakoff’s psychosis describes the chronic cognitive decline resulting from permanent alcohol brain damage that usually appears once Wernicke’s encephalopathy fades.  

At its core, wet brain is caused by thiamine deficiency (vitamin B1). The production of this essential vitamin, which does not occur naturally and is supplied through dietary intake, is damaged by the nutrient deficiencies characteristic of alcohol abuse. According to the National Institute on Alcoholism and Alcohol (NIAA), thiamine deficiency is considered extremely rare in developed nations— except in those suffering from alcohol use disorder (AUD) or human immunodeficiency virus (HIV). It also occasionally occurs in patients who undergo extended intravenous (IV) therapy without concurrent vitamin supplementation.

In even the most robust individuals, chronic alcohol abuse prevents thiamine absorption and depletes crucial reserves of the vitamin stored in the liver. The delicate tissues of the body and brain depend upon thiamine for proper functioning and cannot survive without a regular, healthy supply. Once thiamine levels are depleted, cognitive deficits inevitably appear and irreversible brain damage begins—both of which result in debilitating social and professional consequences as autonomous functioning declines. In order to create the severe physical and neurological damage associated with wet brain, however, alcohol intake must be excessive. Statistical averages suggest that approximately 35 drinks per week for men over a five-year period, and 28 for women over the same time frame, is sufficient to create the onset of the disorder.


Currently, approximately 1.1 to 2.3 million senior citizens struggle with AUDs. Within that population, between 22 and 29 percent of individuals suffering from dementia are alcoholics. Although wet brain was implicated in less than 2.8 percent of reported autopsies, it is estimated that 25 percent of cases were overlooked as a result of failure to use microscopic examination. Further studies concluded that a mere 20 percent of official WKS diagnoses were properly made during life, when compared to subsequent autopsy findings.

The mortality rate associated with wet brain is between 10 and 20 percent, with approximately 80 to 90 percent of survivors fully transitioning from acute Wernicke’s encephalopathy to chronic Korsakoff’s psychosis. In 2015, the National Survey on Drug Use and Health (NSDUH) reported that approximately 15 million Americans age 18 or older suffered from an AUD. Such rampant early abuse sets the stage for the later development of WKS, and paints a grim, highly concerning portrait of the prevalence of alcoholism in American culture.


Although no standardized test exists for diagnosing wet brain, doctors combine an in-depth neurological exam with a comprehensive physical evaluation that includes checking reflexes and overall motor function, testing ocular movement and coordination, and analyzing blood pressure, content, and body temperature. A significant percentage of patients diagnosed with wet brain suffer from an accelerated heart rate— a debilitating symptom called tachycardia. In the acute stage of the disorder, patients may also suffer from noticeable changes in skin tone and texture, as well as a red, inflamed and swollen tongue.

Depending upon whether a person is experiencing Wernicke’s encephalopathy or Korsakoff’s psychosis, the following symptoms may be present:

  • Disorientation and confusion
  • Loss of muscle coordination (ataxia)
  • Obvious cognitive deficits
  • Double vision
  • Visual and auditory hallucinations
  • Impaired ocular movement or incoordination
  • Extreme memory loss (amnesia)
  • Drooping eyelids
  • Uneven gait
  • Coma and/or death


The early diagnosis and treatment of wet brain is critical to achieving favorable treatment outcomes. Wet brain is a potentially life-threatening medical emergency requiring immediate attention and preventative care. The proper administration of thiamine can prevent Wernicke’s encephalopathy from progressing into full-blown WKS, at which point the neurological and structural damage sustained is permanent. Typically, patients are given high doses of thiamine hydrochloride—at least 500mg—administered via infusion for a 30-minute period over the course of two or three days. This treatment is immediately discontinued if no improvement is observed, with responding patients receiving 250mg doses for an additional three to five days.  

Maintaining a healthy, active lifestyle and consuming a diet rich in vitamin B producing foods are also considered a cornerstone of treatment. The following foods should be incorporated into the diet as soon as wet brain is suspected or a proper diagnosis given:

  • Whole grains
  • Bread
  • Spinach
  • Eggs
  • Oranges
  • Milk
  • Kale
  • Lean protein

Although the symptoms of wet brain can be managed and the progression of the disorder controlled to a certain extent if caught early, treatment alone will not eliminate existing cognitive deficits. Wet brain is the result of extensive neurological and physiological damage inflicted by the poison of excessive alcohol consumption and there is no known cure aside from abstinence. It is better to not drink to excess or, ideally, not drink at all, than to face the progressive decline associated with a disorder as painful and debilitating as WKS.

For more related information, check out these articles:

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Springer Neuropsychology Review. The Evolution and Treatment of Korsakoff’s Syndrome. May, 2012.

Journal of Alcohol and Alcoholism. Long-Term Mortality of Patients with an Alcohol-Related Wernicke—Korsakoff Syndrome. March, 2017.

The Journal for Nurse Practitioners (JNP). Alcohol Use in the Elderly and the Risk for Wernicke-Korsakoff Syndrome. Sept, 2010.

International Journal of Experimental and Clinical Pathophysiology and Drug Research. Complete recovery from untreated Wernicke—Korsakoff Syndrome Following Aggressive Thiamine Treatment. March, 2010.

MVP Journal of Medical Sciences. A Case Report on Wernicke-Korsakoff Syndrome. Jan, 2014.