Wernicke–Korsakoff syndrome (WKS), colloquially referred to as wet brain syndrome, is the combined presence of Wernicke encephalopathy (WE) and Korsakoff syndrome. Due to the close relationship between these two disorders, people with either are usually diagnosed with WKS as a single syndrome. It mainly causes vision changes, ataxia and impaired memory. The cause of the disorder is thiamine (vitamin B1) deficiency. This can occur due to eating disorders, malnutrition, and alcohol abuse. These disorders may manifest together or separately. WKS is usually secondary to prolonged alcohol abuse. Wernicke encephalopathy and WKS are most commonly seen in people with an alcohol use disorder. Failure in diagnosis of WE and thus treatment of the disease 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.
Signs and symptoms The syndrome is a combined manifestation of two namesake disorders, Wernicke encephalopathy and Korsakoff syndrome. It involves an acute Wernicke encephalopathy phase, followed by the development of a Korsakoff syndrome phase.
Wernicke encephalopathy WE is characterized by the presence of a triad of symptoms:
Ocular disturbances (ophthalmoplegia) Changes in mental state (confusion) Unsteady stance and gait (ataxia) This triad of symptoms results from a deficiency in vitamin B1, which is an essential coenzyme. The aforementioned changes in mental state occur in approximately 82% of patients; symptoms include confusion, apathy, inability to concentrate, and a decrease in awareness of the immediate situation they are in. If left untreated, WE can lead to coma or death. In about 29% of patients, ocular disturbances consist of nystagmus and paralysis of the lateral rectus muscles or other muscles in the eye. A smaller percentage of patients experience a decrease in reaction time of the pupils to light stimuli and swelling of the optic disc, which may be accompanied by retinal hemorrhage. Finally, the symptoms involving stance and gait occur in about 23% of patients and result from dysfunction in the cerebellum and vestibular system. Other symptoms that have been present in cases of WE are stupor, low blood pressure (hypotension), and elevated heart rate (tachycardia), as well as hypothermia, epileptic seizures and a progressive loss of hearing. Wernicke's encephalopathy has also been reported in non-alcoholic patients, emphasizing that nutritional deficiency, not alcohol itself, can cause the disorder. About 19% of patients have none of the symptoms in the classic triad at first diagnosis of WE; however, usually one or more of the symptoms develops later as the disease progresses.
Korsakoff syndrome The DSM-5 classifies Korsakoff syndrome under Substance/Medication-Induced Major or Mild Neurocognitive Disorders, specifically alcohol-induced amnestic confabulatory. The criteria defined as necessary for diagnosis include prominent amnesia, forgetting quickly, and difficulty learning. Presence of thiamine-deficient encephalopathy can occur in conjunction with these symptoms. Despite the assertion that Korsakoff syndrome must be caused by the use of alcohol, there have been several cases where it has developed from other instances of thiamine deficiency resulting from gross malnutrition due to conditions such as stomach cancer, anorexia nervosa, and gastrectomy. Brain testing shows that Korsakoff patients have greater problems with tasks involving planning and decision-making, linked to prefrontal cortex dysfunction overall.
Cognitive effects Several cases have been documented where Wernicke–Korsakoff syndrome has been seen on a large scale. In 1947, 52 cases of WKS were documented in a prisoner of war hospital in Singapore where the prisoners' diets included less than 1 mg of thiamine per day. Such cases provide an opportunity to gain an understanding of what effects this syndrome has on cognition. In this particular case, cognitive symptoms included insomnia, anxiety, difficulties in concentration, loss of memory for the immediate past, and gradual degeneration of mental state consisting of confusion, confabulation, and hallucinations. In other cases of WKS, cognitive effects such as severely disrupted speech, giddiness, and heavy-headedness have been documented. PET scans of patients with Wernicke–Korsakoff syndrome have shown decreased activity in areas such as the thalamus and mammillary bodies, which are important for memory and coordination. (Reed 2003.) In addition to this, it has been noted that some patients displayed an inability to focus, and it was difficult to obtain patients' attention. In a study conducted in 2003 by Brand et al. on the cognitive effects of WKS, the researchers used a neuropsychological test battery that included tests of intelligence, speed of information processing, memory, executive function and cognitive estimation. They found that subjects with WKS showed impairments across all aspects of the test battery, with the most pronounced deficits observed in cognitive estimation tasks. These tasks required participants to estimate physical properties such as size, weight, quantity, or time (for example, estimating the average length of a shower). Patients with WKS performed worse than control participants on all tasks in this category. Estimations involving time proved to be the most difficult, while those involving quantity were the easiest. The study also included a category for “bizarre” responses, defined as answers that fell far outside the typical range of expected values. Individuals with Wernicke–Korsakoff syndrome frequently exhibit disorientation and confabulation, often generating fabricated explanations to compensate for memory deficits. (Schnider2023). WKS patients did give answers that could fall into such a category, such as 15 seconds or 1 hour for the estimated length of a shower, or 4 kg or 15 tonnes as the weight of a car.
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