Wernicke–Korsakoff syndrome (WKS), also called wet brain, is a very dangerous and under-diagnosed condition most commonly seen in in people who chronically misuse alcohol.
Korsakoff’s psychosis, and alcoholic encephalopathy is the combined presence of Wernicke’s encephalopathy and Korsakoff’s syndrome. Due to the close relationship between these two disorders, people suffering from both are usually diagnosed with WKS, as a single syndrome. [1]
WKS is caused by thiamine (vitamin B1) deficiency. Strong evidence suggests that ethanol interferes directly with thiamine uptake in the gastrointestinal tract. Ethanol also disrupts thiamine storage in the liver and the transformation of thiamine into its active form,[2] therefore chronic drinkers have a higher risk for thiamine deficiency – even though they may never develop WKS. The neurotoxic effects of alcohol may also play a role, and there is new research that underscores a potential genetic component as well. [3]
Some studies have suggested that WKS impacts approximately 12.5% of long-term alcoholics[4] – however, only 20% of these are identified before death. That means that 80% of people with WKS may never receive a diagnosis or treatment. The failure to diagnosis WKS leads to death in approximately 20% of cases, while 75% are left with permanent brain damage associated with WKS. Of those affected, 25% require long-term institutionalization in order to receive effective care.[5]
Some Facts:
- Alcohol-related brain damage may contribute to between 10% and 24% of all cases of dementia.
- The incidence of WKS has been reported to be rising in recent years.
- Prevalence rates are likely to be higher in areas of socio-economic deprivation and in those aged 50-60 years. For example, WKS is higher among those who are homeless.
Risk Factors:[6]
The major risk factors for developing WKS are malnourishment and chronic alcoholism. Other risk factors for WKS include:
- being unable to afford medical care and proper food
- undergoing kidney dialysis, which reduces vitamin B1 absorption
- acquired immunodeficiency syndrome (AIDS), which makes an individual more likely to develop conditions that lead to vitamin B1 shortage
Presentation:[7]
Any person with alcohol misuse who experiences confusion, nausea and vomiting, fatigue, weakness or apathy should be considered at high risk of WKS and treated appropriately.
Signs and Symptoms:
- Vision changes
- Double vision
- Eye movement abnormalities
- Eyelid drooping
- Loss of muscle coordination
- Unsteady, uncoordinated walking
- Loss of memory, which can be profound
- Inability to form new memories
- Hallucinations
Additional Cognitive Features:
- amnesia for events that happen after the onset of the disorder
- difficulty understanding the meaning of information
- difficulty putting words into context
- hallucinations
- exaggerated storytelling (confabulation)
Treatment:
Early intervention increases the likelihood of positive outcomes and to prevent irreversible damage to the brain. In fact, Australia had one of the highest prevalence rates for WKS. In 1991 they began to fortify bread with Thiamine and the incidence of WKS has declined. [8]
There are advocates who suggest that thiamine could be added to beer. The rationale is that some alcoholics do not eat enough food- fortified or otherwise to benefit from thiamine enriched products. This is a controversial approach for several reasons. Firstly, there is concern that fortified beer would only encourage more harmful usage. (Probably the same people who think sex education leads to teenage pregnancy). The real problem with fortifying beer is that it is unclear how much thiamine could actually be absorbed through the vehicle of alcohol since alcohol inhibits the absorption of thiamine.
Despite a number of studies, there is no consensus on the optimal dose of thiamine, its preparation form, duration of treatment, or the number of daily doses. Typically, it is given via intravenous during medical detox followed by daily oral thiamine (100 mg) following discharge. People with WKS need to work closely with their physicians to ensure the right treatment and dosage.
What can I do?
-
Learn about the signs and symptoms of WKS
-
If you suspect WKS in yourself or someone else, seek medical advice.
-
Share this information with others. Help end unnecessary death and suffering caused by WKS.
[1] “MedlinePlus – Wernicke-Korsakoff syndrome”. Nlm.nih.gov.
[2] Todd K., Hazell A., Butterworth R. (1999). “Alcohol thiamine interactions: an update on the pathogenesis of wernicke encephalopathy”. Addiction Biology 4: 261–272.
[3] Thompson, A. (2000). Alcohol & Alcoholism Vol. 35, Suppl: 2-7.
[4] http://www.medicine.virginia.edu/clinical/departments/medicine/divisions/digestive-health/nutrition-support-team/nutrition-articles/ThomsonArticle.pdf. Retrieved 2015-07-22.
[5] Thomson A., Marshall E. (2006). “The natural history and pathophysiology of Wernicke’s encephalopathy and Korsakoff’s psychosis”. Alcohol & Alcoholism 41 (2): 151–158.
[6] http://www.healthline.com/health/wernicke-korsakoff-syndrome#Riskfactors2. Retrieved 2015-07-22.
[7] http://patient.info/doctor/wernicke-korsakoff-syndrome. Retrieved 2015-07-22.
[8] Truswell A. (2000). Australian experience with the Wernicke-Korsakoff syndrome. Addiction;95:829-32.
Written by Carlene Dingwall
Mental Health, Substance Use and HIV/HCV Working Group
