Wernicke-Korsakoff syndrome is a co-occurrence of two brain disorders: Wernicke encephalopathy and Korsakoff syndrome. Because of the close relationship between these disorders, people with either condition are diagnosed with Wernicke-Kosakoff syndrome as a single syndrome. The primary cause of this type of brain disorder is thiamine deficiency, which in turn can cause a group of disorders including beriberi, Wernicke encephalopathy and Korsakoff psychosis, which may occur together or separately. Wernicke-Korsakoff syndrome is usually a secondary result of alcohol abuse, which in turn can cause significant changes in vision, movement disorders and memory impairment. Alcoholics are the most common people to develop Wernicke encephalopathy and Wernicke-Korsakoff syndrome, and only about 20% of these cases are diagnosed before death. Failure to diagnose and thus treat this type of condition is the main cause of death in about 20% of cases. While 75% of patients may suffer from permanent brain damage associated with this syndrome. As for those affected, 25% of them need the intervention of the concerned institutions for the long term to provide them with the necessary and effective care. This syndrome appears as a result of the presence of two disorders with the same name - Wernicke's encephalopathy and Korsakoff's psychosis. This syndrome includes two stages: an acute stage of Wernicke's encephalopathy followed by the development of a chronic stage of Korsakoff's syndrome. This type of disorder is characterized by the presence of three symptoms: These three symptoms result from a severe deficiency of an essential coenzyme in the body, which is vitamin D. The above-mentioned changes in the psychological state occur in about 82% of the general symptoms that patients suffer from as a whole, and this ranges from confusion and apathy, inability to concentrate and decreased ability to act immediately in situations that require it. The condition may end in a coma or death if these symptoms are left untreated. In about 29% of patients, eye disorders are represented by nystagmus and paralysis of the lateral rectus muscles or other muscles in the eye. While there is a smaller percentage of patients The syndrome is characterized by a marked decrease in the normal reaction time required for visual stimuli in addition to swelling of the optic disc, which may often be accompanied by retinal hemorrhage. Finally, symptoms involving unstable posture and gait may occur in about 23% of patients and are due to dysfunction of the cerebellum and vestibular system. In addition to the symptoms mentioned, the person with the syndrome suffers from a clear state of stupor, low blood pressure, high heart rate, low body temperature, seizures and progressive hearing loss. The syndrome is described as an acute onset of severe memory impairment without any obvious impairment in the person's thinking or learning abilities. The Diagnostic and Statistical Manual of Mental Disorders lists a set of criteria for diagnosing Korsakoff syndrome, which includes a set of symptoms, the most important of which are the following: In addition to the presence of one of these symptoms: In addition, the DSM-IV indicates that the daily activities and functions of the affected person will be affected by memory deficits, and that the phase in which the affected person loses memory must occur outside of times when the individual is in a state of delirium, intoxication or trying to quit The criteria used to diagnose the syndrome maintain the need for evidence that the amnesia in the sufferer is the result of alcohol use. Although alcohol is considered the main cause of Korsakoff syndrome as mentioned above, other conditions have been proven to be the cause, including: Thiamine deficiency, which is caused by malnutrition due to many conditions such as stomach cancer, anorexia nervosa and gastrectomy. Wernicke-Korsakoff syndrome has been diagnosed on a large scale. In 1947, 52 patients were diagnosed in a hospital in Singapore where the prisoners’ diets contained less than 1 mg of thiamine per day. Thus, such cases have provided an opportunity to understand the nature of the effects of this syndrome on the cognitive and perceptual abilities of the sufferer as a whole. In this particular case, the sufferer suffers from insomnia, anxiety, difficulties in concentration, loss of memory for the recent past, and a gradual decline in psychological status, including confusion, contemplation and hallucinations. In other cases, the syndrome has caused other cognitive symptoms, including: severe speech impairment, Dizziness, and a heavy head. In addition, some patients have been observed to suffer from a loss of ability to concentrate and the inability of others to attract the attention of these patients due to their distraction. In a study conducted in 2003 by Brand on the cognitive effects caused by the syndrome, researchers used a neuropsychological test battery that included tests of intelligence, data processing speed, memory, executive function, and cognitive estimation. Researchers found that patients with Wernicke-Korsakoff syndrome showed significant impairment in all aspects of the tests of this battery, but most notably on cognitive estimation tasks. This task requires subjects to estimate physical qualities such as size, weight, quantity, and time for a particular item. Patients with this syndrome performed poorly on these tasks compared to the normal group. Patients found that estimates related to time were more difficult for them than estimates related to quantity, which were easier for them to estimate. In addition, the study included a category for classifying “odd” answers, meaning any answer that was very far from the normal range of expected responses. Patients with the syndrome gave answers that could fall into this category, including answers such as 15 seconds or one hour for the estimated length of a shower, or 4 kg or 15 tons for a car. Memory loss in patients with Wernicke-Kosakoff syndrome includes both retrograde amnesia and anterograde amnesia. Retrograde amnesia is represented by the inability of patients with the syndrome to recall memories or recognize information related to recent public events, while anterograde amnesia is represented by the patient's inability to perform tasks related to the ability to encode or remember words or faces as well as semantic learning tasks. Patients with the syndrome have also shown difficulties in the ability to memorize, as evidenced by their performance deficits on the Wisconsin Card Sorting Test. Retrograde amnesia associated with Wernicke-Kosakoff syndrome can extend for a period ranging from twenty to thirty years under a chronological gradient, such that the patient can retrieve past memories better than recent memories. It has been widely agreed that the brain bodies responsible for the memory impairment associated with the syndrome are the mammillary bodies and the thalamic regions. Despite the memory deficits mentioned above, unconscious memory functions appear to be almost intact in patients with the syndrome. This has been demonstrated by psychological preparation tests. Other studies have shown deficits in recognition memory and motivational and reward retrieval in patients with Wernicke-Korsakoff syndrome. Deficits in motivational and reward functions were demonstrated by Oskar-Berman and Pulaski who presented patients with reinforcements for some stimuli but not others, and then asked patients to discriminate rewarding stimuli from non-rewarding stimuli. Patients with the syndrome showed significant deficits on this task. Researchers have also successfully demonstrated deficits in recognition memory by having patients make a yes/no decision as to whether a stimulus was familiar or novel, and patients in this study showed significant deficits in their ability to perform this task as well. Spontaneous compromises refer to incorrect memories that the patient believes to be correct, and may arise spontaneously without any provocation. Enriched distortions can occur when the patient is committed to providing a response, which may occur in test settings. Spontaneous compromises that are displayed in WKS are thought to result from a deficit in source memory, where they are unable to recall spatial and contextual information of the event, and thus may They use old or inappropriate memory traces to fill in the inaccessible information. It has also been suggested that this behavior may be due to executive dysfunction where they are unable to inhibit incorrect memories or are unable to divert their attention from the incorrect response. Wernicke-Korsakoff syndrome is commonly found in alcoholics and is caused by a deficiency of thiamine. It is generally agreed that the encephalitis in Wernicke syndrome is caused by severe thiamine deficiency. Thiamine pyrophosphate is the active metabolic form of thiamine and plays an important role as a cofactor or enzyme in glucose metabolism. The enzymes that depend primarily on pyrophosphate are found in the citric acid cycle, also known as the Krebs cycle, where they catalyze the oxidation of pyruvate, alpha-ketoglucoate, and branched-chain amino acids. Therefore, what increases glucose metabolism will certainly exacerbate clinical thiamine deficiency. As mentioned earlier, Wernicke-Korsakoff syndrome in the United States is particularly prevalent in those who are malnourished. Alcoholics, long-term IV patients without vitamin B1 supplements, patients undergoing gastric bypass surgery, or hunger strikers. In some areas, thiamine deficiency has been noted in severe malnutrition, particularly in diets high in white rice, which is a thiamine-deficient food. The neurological disease resulting from thiamine deficiency is called beriberi. In people with subclinical thiamine deficiency, a large dose of glucose can precipitate the onset of overt encephalopathy. Wernicke-Korsakoff syndrome in alcoholics is associated with atrophy/infarction of certain brain regions, especially the mammillary bodies. Other regions include the anterior region of the thalamus, the medial hypothalamus, the basal forebrain, the medial and lateral Rajesh nuclei, and the cerebellum. One isolated study has linked susceptibility to this syndrome to inherited deficiency of transketolase, an enzyme that requires thiamine as a cofactor. The fact that gastrointestinal surgery contributes to the development of Wernicke-Korsakoff syndrome was demonstrated by a study of three patients who had recently undergone gastrectomy. These patients later developed Wernicke-Korsakoff syndrome but were not alcoholics and had no history of food deprivation or malnutrition. Wernicke-Korsakoff syndrome developed within two to twenty years after surgery. There were minor dietary changes that contributed to the development of Wernicke-Korsakoff syndrome but in general the underlying cause was poor absorption of thiamine from the gastrointestinal tract. Therefore, it is important to ensure that patients who undergo gastrectomy are fully aware of proper dietary habits and to monitor the amount of thiamine they consume. In addition, early diagnosis of Wernicke-Korsakoff syndrome, if it develops, is very important. Strong evidence indicates that ethanol directly interferes with the absorption of thiamine in the gastrointestinal tract. Ethanol also disrupts the storage of thiamine in the liver and the conversion of thiamine to its active isotope. The role of alcohol consumption in the development of Wernicke-Korsakoff syndrome has been experimentally agreed upon. Wernicke-Korsakoff syndrome was demonstrated by using rats that were exposed to alcohol and reduced their thymine levels by providing them with a diet containing little thymine. In particular, scientific studies have shown that clinical symptoms of neurological problems resulting from thymine deficiency develop faster in rats that consumed alcohol and a diet deficient in thymine than in rats that did not consume alcohol. In another study, rats that were chronically and continuously fed alcohol were found to have significantly reduced thymine stores in the liver compared to rats that were given alcohol regularly and under supervision. This provides an explanation for why thymine deficiency and Wernicke-Korsakoff syndrome are higher in alcoholics who suffer from liver cirrhosis. The brain atrophy associated with Wernicke-Korsakoff syndrome occurs in the following areas: mammillary bodies, thalamus, central gray, walls of the third ventricle, floor of the fourth ventricle, cerebellum and frontal lobe. In addition to the observed destruction in these areas, there are some reports of damage to the cerebral cortex, although it has been noted that this may be due to direct toxic effects. Alcoholic thymine deficiency has been linked to the underlying cause of Wernicke-Korsakoff syndrome. The amnesia associated with this syndrome is due to atrophy of the diencephalic regions, similar to the amnesia seen in cases of midtemporal lobe injury. It has been suggested that memory impairment can occur as a result of damage to any part of the mammillary-thalamic pathway, which explains how Wernicke-Korsakoff syndrome develops in patients with damage to the thalamus or mammillary bodies. The diagnosis of Wernicke-Korsakoff syndrome is based on clinical impression and is sometimes confirmed by formal neuropsychological evaluation. The encephalopathy associated with Wernicke syndrome presents with ataxia, nystagmus, and Korsakoff psychosis with retrograde and anterograde amnesia. Often, because of the thymine deficiency and resulting cerebral edema in Korsakoff syndrome, patients have marked regression of the mammillary bodies. Thymine is an important coenzyme essential for carbohydrate metabolism and is also Regulator of the osmotic gradient. Thiamine deficiency may cause swelling of the intracellular space and local disturbance of the blood-brain membrane. The blood-brain membrane is sensitive to changes in electrolytes and pressure and cerebral edema can be toxic. This occurs in Wernicke syndrome particularly in the mammillary bodies, the midbrain, the tectum of the midbrain and the central gray. Affected patients may also have aversion to sunlight and may wish to stay indoors with the lights off. The mechanism of this degeneration is unknown, but it supports the current neurological theory that the mammillary bodies play a role in various “memory circuits” within the brain. An example of a memory circuit is the Papez circuit. Axial image shows signal in the central gray matter and the tectum of the midbrain. Axial image shows signal indicating limited diffusion in the dorsal thalamus. Axial FLAIR MRI shows signal in the dorsal thalamus, which is common in Wernicke syndrome-associated encephalopathy. This patient was nearly comatose when he was started on intravenous thiamine; he responded well but was left with some deficits associated with the syndrome. Korsakoff. The appearance of Wernicke's encephalopathy is a medical emergency, and thiamine should be started immediately if symptoms of the disease are suspected; This is because thiamine prevents the disease from developing into Wernicke-Korsakoff syndrome and reduces the severity of the disease. Treatment can alleviate the disability resulting from the disease and its symptoms, but it cannot return the patient to normal or reverse the existing deficiencies. At least 80% of patients continue to show symptoms of Wernicke-Korsakoff syndrome despite continuing treatment. Patients suffering from Wernicke encephalopathy should be given the minimum dose of thiamine hydrochloride (which is equivalent to 500 mg intravenously over 30 minutes for two to three days. If the patient does not respond, treatment should be stopped immediately. As for patients who respond to treatment, thiamine hydrochloride is continued, but with a modification in the amount and duration of the dose to 250 mg for three to five days intravenously or intramuscularly. In addition, another method used in treatment is the use of a banana bag, which is a bag containing vitamins and minerals in addition to thiamine) given intravenously. As previously explained, Korsakoff syndrome is often associated with Wernicke-Korsakoff encephalopathy unless Wernicke-Korsakoff encephalopathy is treated promptly with thiamine (this will prevent the disease from developing into Korsakoff syndrome), so the appropriate dose of thiamine must be given at the appropriate time. On the other hand, a study on Wernicke-Korsakoff syndrome showed that adherence to thiamine (this led to significant improvements in mental status after only two to three weeks of treatment, which gives hope that Wernicke-Korsakoff encephalopathy does not necessarily develop into Wernicke-Korsakoff syndrome. At the same time, in order to reduce the risk of developing Wernicke-Korsakoff syndrome, it is important to limit the consumption of alcohol and alcoholic beverages and follow a healthy diet in order to meet the body's needs for proper nutrition, which works together with thiamine (this will reduce the chance of developing Wernicke-Korsakoff syndrome). This method may also help in getting rid of alcohol addiction in people who are unable to quit alcoholism. Internationally, the prevalence of Wernicke-Korsakoff encephalopathy is relatively stable, anywhere between Zero and two percent. However, there are certain groups that have higher rates of Wernicke-Korsakoff syndrome, especially homeless people, the elderly, and mentally ill patients in institutions. In addition, studies indicate that the prevalence of Wernicke-Korsakoff syndrome is not related to the rate of alcohol consumption per capita. For example, in France, a country well known for its wine consumption and production, the prevalence of the disease was only 0.4% in 1994, while in Australia the prevalence of the disease was 2.8%. Carl Wernicke discovered Wernicke encephalopathy in 1881. During his first diagnosis of the disease, he noted the following symptoms: paralysis of eye movements, ataxia, and mental confusion. He also noted bleeding in the gray matter around the third and fourth ventricles in the cerebral aqueduct. In addition, he noted brain atrophy after dissecting a patient with the disease. On the other hand, Wernicke believed that the bleeding was caused by inflammation, so he called the disease epidural hemorrhagic myelitis. Later, he found that The cause of Wernicke's encephalopathy and Korsakoff's syndrome is the same. Sergei Korsakoff was a Russian physician after whom "Korsakoff's syndrome" was named. In the late 19th century, Korsakoff was following long-term alcoholic patients and began to notice a decline in their memory function. At the 13th International Medical Congress in Moscow in 1897, Korsakoff presented a report entitled: "A special form of mental illness with degenerative neuritis." It was after this report that the term "Korsakoff's syndrome" was coined. Although Wernicke's encephalopathy and Korsakoff's syndrome were discovered separately, they are usually referred to under the same name, Wernicke-Korsakoff syndrome, due to the fact that they are part of the same cause and because the onset of Korsakoff's syndrome usually follows Wernicke's encephalopathy if left untreated. A famous case study was written about by Oliver Sacks, in the story "The Lost Sailor," in his book "The Man Who Mistook His Wife for a Hat."