Neurological cause of psychogenic amnesia is controversial. Even in cases of organic amnesia, where there is lesion or structural damage to the brain, caution must still be taken in defining causation, as only damage to areas of the brain crucial to memory processing is it possible to result in memory impairment. Organic causes of amnesia can be difficult to detect, and often both organic cause and psychological triggers can be entangled. Failure to find an organic cause may result in the diagnosis that the amnesia is psychological, however it is possible that some organic causes may fall below a threshold of detection, while other neurological ails are thought to be unequivocally organic (such as a migraine) even though no functional damage is evident. Possible malingering must also be taken into account. Some researchers have cautioned against psychogenic amnesia becoming a 'wastebasket' diagnosis when organic amnesia is not apparent. Other researchers have hastened to defend the notion of psychogenic amnesia and its right not to be dismissed as a clinical disorder. Diagnoses of psychogenic amnesia have dropped since agreement in the field of transient global amnesia, suggesting some over diagnosis at least. Speculation also exists about psychogenic amnesia due to its similarities with 'pure retrograde amnesia', as both share similar retrograde loss of memory. Also, although no functional damage or brain lesions are evident in the case of pure retrograde amnesia, unlike psychogenic amnesia it is not thought that purely psychological or 'psychogenic triggers' are relevant to pure retrograde amnesia. Psychological triggers such as emotional stress are common in everyday life, yet pure retrograde amnesia is considered very rare. Also the potential for organic damage to fall below threshold of being identified does not necessarily mean it is not present, and it is highly likely that both psychological factors and organic cause exist in pure retrograde amnesia.

Amnesia is partial or complete loss of memory that goes beyond mere forgetting. Often it is temporary and involves only part of a person's experience. Amnesia is often caused by an injury to the brain, for instance after a blow to the head, and sometimes by psychological trauma. Anterograde amnesia is a failure to remember new experiences that occur after damage to the brain; retrograde amnesia is the loss of memories of events that occurred before a trauma or injury. For a memory to become permanent (consolidated), there must be a persistent change in the strength of connections between particular neurons in the brain. Anterograde amnesia can occur because this consolidation process is disrupted; retrograde amnesia can result either from damage to the site of memory storage or from a disruption in the mechanisms by which memories can be retrieved from their stores. Many specific types of amnesia are recognized, including:

- Childhood amnesia is the normal inability to recall memories from the first three years of life. Sigmund Freud observed that not only do humans not remember anything from birth to three years, but they also have “spotty” recollection of anything occurring from three to seven years of age. There are various theories as to why this occurs: some believe that language development is important for efficient storage of long-term memories; others believe that early memories do not persist because the brain is still developing.

- A fugue state, formally dissociative fugue, is a rare condition precipitated by a stressful episode. It is characterized by episode(s) of traveling away from home and creating a new identity.

The form of amnesia that is linked with recovered memories is dissociative amnesia (formerly known as psychogenic amnesia). This results from a psychological cause, not by direct damage to the brain, and is a loss of memory of significant personal information, usually about traumatic or extremely stressful events. Usually this is seen as a gap or gaps in recall for aspects of someone's life history, but with severe acute trauma, such as during wartime, there can be a sudden acute onset of symptoms.

Alzheimer's disease (AD), which is known to be associated with frontal lobe dysfunction, is implicated as a cause of source amnesia. In laboratory conditions, one study found source monitoring to be so poor that the AD participants were correctly performing source memory attributions at approximately chance. This lack of ability to attribute the source of memories is likely related to AD patients' deficits in reality monitoring. Reality monitoring, the process of distinguishing whether information originated from an external or an internal source, relies on judgement processes to examine the qualitative characteristics of the information in order to determine if the information was real or imagined. It appears that it is this process that is experiencing the dysfunction, which causes mild confabulation in some AD patients, as well as being related to the source amnesia experienced in some individuals with AD.

Psychogenic amnesia is defined by the presence of retrograde amnesia (the inability to retrieve stored memories leading up to the onset of amnesia), and an absence of anterograde amnesia (the inability to form new long term memories). Access to episodic memory can be impeded, while the degree of impairment to short term memory, semantic memory and procedural memory is thought to vary among cases. If other memory processes are affected, they are usually much less severely affected than retrograde autobiographical memory, which is taken as the hallmark of psychogenic amnesia. However the wide variability of memory impairment among cases of psychogenic amnesia raises questions as to its true neuropsychological criteria, as despite intense study of a wide range of cases there is little consensus of which memory deficits are specific to psychogenic amnesia.

Past literature has suggested psychogenic amnesia can be 'situation-specific' or 'global-transient', the former referring to memory loss for a particular incident, and the latter relating to large retrograde amnesic gaps of up to many years in personal identity. The most commonly cited examples of global-transient psychogenic amnesia are 'fugue states', of which there is a sudden retrograde loss of autobiographical memory resulting in impairment of personal identity and usually accompanied by a period of wandering. Suspected cases of psychogenic amnesia have been heavily reported throughout the literature since 1935 where it was reported by Abeles and Schilder. There are many clinical anecdotes of psychogenic or dissociative amnesia attributed to stressor ranging from cases of child sexual abuse to soldiers returning from combat.

It is normal to have some level of memory distrust, or the lack of trusting in one's own memory. This may occur when speaking with your parents about your childhood, for example. However it seems that everyone has their own level of memory distrust, and memory distrust syndrome seems to be a severe case.

The direct cause is unknown; however, it is possibly a defense or coping mechanism to a preexisting condition that would alter one's memory. This could involve frontal lobe lesions, Alzheimer's disease, amnesia, dementia, or other conditions. Any condition that would alter either existing memories or the formation of new memories could cause a coping scheme such as memory distrust syndrome. Alternatively, an individual may have learned over time to not trust their own memory from conditioning, and as such the individual would develop a defense mechanism to remove themselves from potential embarrassment.

RA has been found among alcohol-dependent patients who suffer from Korsakoff's syndrome. Korsakoff's syndrome patients suffer from retrograde amnesia due to a thiamine deficiency (lack of vitamin B1). Also, chronic alcohol use disorders are associated with a decrease in volume of the left and right hippocampus.

These patients' regular diet consists mostly of hard alcohol intake, which lacks the necessary nutrients for healthy development and maintenance. Therefore, after a prolonged time consuming primarily alcohol, these people undergo memory difficulties and ultimately suffer from RA. However, some of the drawback of using Korsakoff patients to study RA is the progressive nature of the illness and the unknown time of onset.

The main symptom of memory distrust syndrome is the lack of belief in one's own memory, however this comes with the side effect of using outside sources for information. The individual may have their own memory, but will readily change it depending on chosen outside sources. The memories that they have may be correct, but due to their distrust they will still alter their belief of what is true if contrary information is suggested.

For example, a person has a memory of a house and recalls it to be white. Then, a trusted family member begins talking with them and suggests that it was red instead. The afflicted individual will then believe the house was red despite their recollection of it being white. It is unknown if the person's memory of the house is permanently altered; however, they will say that the house was red regardless of the memory's condition.

Also, this does not necessarily allow for confabulatory memory fabrication. Currently it is not believed that an afflicted individual will readily believe an outside source on a memory of which the person is not involved, such as a randomly shared story. This further suggests that memory distrust syndrome solely alters the individual's currently retrievable memories, and not randomized information.

Schizophrenia is associated with episodic memory deficits often characterized by a confusion of internal stimuli and real events. It appears that individuals with schizophrenia often display failures in monitoring/remembering the source of information, especially for self-generated items – that is, they display source amnesia. This is a stable trait in this disease – one experiment found that over a two-year period, an individual's rate of source attributing errors was maintained, despite fluctuations in medication status and the individual's symptoms. This effect is possibly due to the malformation of associations among aspects of an episode needed for remembering its source; one neuroimaging study found that individuals with schizophrenia had lower activation of areas associated with source memory.

Individuals with schizophrenia who display source memory deficits often do so due to reality-monitoring dysfunction, which is a contributing factor towards the hallucinations that characterize the disorder. One study found that schizophrenia patients were not only slower, but also less accurate, at tasks involving reality-monitoring. The hallucinations that characterize schizophrenia are a result of deficit in reality monitoring – they exhibit an inability to differentiate between internally and externally derived information. Overall, there is evidence of a relationship between source monitoring errors and the disorganized thinking that characterizes those who have schizophrenia in that there is a strong tendency for those people with hallucinations to attribute their internally generated events (i.e.: hallucinations and delusions) to an external source (e.g., the experimenter). That is, schizophrenia is characterized by failing to encode themselves as the source of the idea, compounded by attributing these ideas/beliefs to an external source, all of which leads to those individuals with schizophrenia exhibiting behaviours typical of those with source amnesia; they misattribute the source of their knowledge, ideas, or beliefs.

Traumatic brain injury (TBI), also known as post-traumatic amnesia, occurs from an external force that causes structural damage to the brain, such as a sharp blow to the head, a diffuse axonal injury, or childhood brain damage (e.g., shaken baby syndrome). In cases of sudden rapid acceleration, the brain continues moving around in the skull, harming brain tissue as it hits internal protrusions.

TBI varies according to impact of external forces, location of structural damage, and severity of damage ranging from mild to severe. Retrograde amnesia can be one of the many consequences of brain injury but it is important to note that it is not always the outcome of TBI. An example of a subgroup of people who are often exposed to TBI are individuals who are involved in high-contact sports. Research on football players takes a closer look at some of the implications to their high-contact activities. Enduring consistent head injuries can have an effect on the neural consolidation of memory.

Specific cases, such as that of patient ML, support the evidence that severe blows to the head can cause the onset of RA. In this specific case there was an onset of isolated RA following a severe head injury. The brain damage did not affect the person's ability to form new memories. Therefore, the idea that specific sections of retrograde memory are independent of anterograde is supported. Normally, there is a very gradual recovery, however, a dense period of amnesia immediately preceding the trauma usually persists.

Childhood amnesia, also called infantile amnesia, is the inability of adults to retrieve episodic memories which are memories of specific events (times, places, associated emotions, and other contextual who, what, when, and where) before the age of 2–4 years, as well as the period before age 10 of which adults retain fewer memories than might otherwise be expected given the passage of time. The development of a cognitive self is also thought by some to have an effect on encoding and storing early memories. Some research has demonstrated that children can remember events from the age of 1, but that these memories may decline as children get older.

Most psychologists differ in defining the offset of childhood amnesia. Some define it as the age from which a first memory can be retrieved. This is usually at the age of 3 or 4, but it can range from 2 to 8 years. Changes in encoding, storage and retrieval of memories during early childhood are all important when considering childhood amnesia. Some other research shows differences between gender and culture, which is implicated in the development of language. Childhood amnesia is particularly important to consider in regard to false memories and the development of the brain in early years. Proposed explanations of childhood amnesia are Freud's trauma theory, neurological development, development of the cognitive self, emotion and language.

"Betrayal Trauma Theory" proposes that in cases of childhood abuse, dissociative amnesia is an adaptive response, and that “victims may need to remain unaware of the trauma not to reduce suffering but rather to promote survival.”

When stress interferes with memory, it is possible that some of the memory is kept by a system that records emotional experience, but there is no symbolic placement of it in time or space.

Traumatic memories are retrieved, at least at first, in the form of dissociated mental imprints of the affective and sensory elements of the traumatic experience. Clients have reported the slow emergence of a personal narrative that can be considered explicit (conscious) memory.

Psychiatrist Bessel van der Kolk divided the effects of traumas on memory functions into four sets

- traumatic amnesia; this involves the loss of memories of traumatic experiences. The younger the subject and the longer the traumatic event is, the greater the chance of significant amnesia. He stated that subsequent retrieval of memories after traumatic amnesia is well documented in the literature, with documented examples following natural disasters and accidents, in combat soldiers, in victims of kidnapping, torture and concentration camp experiences, in victims of physical and sexual abuse, and in people who have committed murder.

- global memory impairment; this makes it difficult for subjects to construct an accurate account of their present and past history. "The combination of lack of autobiographical memory, continued dissociation and of meaning schemes that include victimization, helplessness and betrayal, is likely to make these individuals vulnerable to suggestion and to the construction of explanations for their trauma-related affects that may bear little relationship to the actual realities of their lives"

- dissociative processes; this refers to memories being stored as fragments and not as unitary wholes.

- traumatic memories’ sensorimotor organization. Not being able to integrate traumatic memories seems to be linked to posttraumatic stress disorder (PTSD).

According to van der Kolk, memories of highly significant events are usually accurate and stable over time; aspects of traumatic experiences appear to get stuck in the mind, unaltered by time passing or experiences that may follow. The imprints of traumatic experiences appear to be different from those of nontraumatic events, perhaps because of alterations in attentional focusing or the fact that extreme emotional arousal interferes with memory. van der Kolk and Fisler's hypothesis is that under extreme stress, the memory categorization system based in the hippocampus fails, with these memories kept as emotional and sensory states. When these traces are remembered and put into a personal narrative, they are subject to being condensed, contaminated and embellished upon.

When there is inadequate recovery time between stressful situations, alterations may occur to the stress response system, some of which may be irreversible, and cause pathological responses, which may include memory loss, learning deficits and other maladaptive symptoms. In animal studies, high levels of cortisol can cause hippocampal damage, which may cause short-term memory deficits; in humans, MRI studies have shown reduced hippocampal volumes in combat veterans with PTSD, adults with posttraumatic symptoms and survivors of repeated childhood sexual or physical abuse. Trauma may also interfere with implicit memory, where periods of avoidance may be interrupted by intrusive emotional occurrences with no story to guide them. A difficult issue is whether those presumably abused accurately recall their experiences.

Fragmentation of memory is a type of memory disruption pertaining to the flaws or irregularities in sequences of memories, "coherence, and content” in the narrative or story of the event. During a traumatic experience, memories can be encoded irregularly which creates imperfections in the memory. It is also described as a memory that has been jumbled, confused, or repeated unnecessarily.

Fragmentation of memory is a memory disorder in when an individual is unable to associate the context of the memories to their autobiographical (episodic) memory. The explicit facts and details of the events may be known to the person (semantic memory). However, the facts of the events retrieve none of the effective and somatic elements of the experience. Therefore, the emotional and personal content of the memories can't be associated with the rest of the memory. Fragmentation of memory can occur for relatively recent events as well.

The impaired person usually suffers from physical damage to or underdevelopment of the hippocampus. This may be due to a genetic disorder or be the result of trauma, such as post-traumatic stress disorder. Brain dysfunction often has other related consequences, such as oversensitivity to some stimuli, impulsiveness, lack of direction in life, occasional aggressiveness, a distorted perception of oneself, and impaired ability to empathize with others, which is usually masked.

Anterograde amnesia can also be caused by alcohol intoxication, a phenomenon commonly known as a blackout. Studies show rapid rises in blood alcohol concentration over a short period of time severely impair or in some cases completely block the brain's ability to transfer short-term memories created during the period of intoxication to long-term memory for storage and later retrieval. Such rapid rises are caused by drinking large amounts of alcohol in short periods of time, especially on an empty stomach, as the dilution of alcohol by food slows the absorption of alcohol. Alcohol-related anterograde amnesia is directly related to the rate of consumption of alcohol (and is often associated with binge drinking), and not just the total amount of alcohol consumed in a drinking episode. Test subjects have been found not to experience amnesia when drinking slowly, despite being heavily intoxicated by the end of the experiment. When alcohol is consumed at a rapid rate, the point at which most healthy people's long-term memory creation starts to fail usually occurs at approximately 0.20% BAC, but can be reached as low as 0.14% BAC for inexperienced drinkers. The exact duration of these blackout periods is hard to determine, because most people fall asleep before they end. Upon reaching sobriety, usually after waking, long-term memory creation is completely restored.

Chronic alcoholism often leads to a thiamine (vitamin B) deficiency in the brain, causing Korsakoff's syndrome, a neurological disorder which is generally preceded by an acute neurological condition known as Wernicke's encephalopathy (WE).

The memory impairment that is pathognomonic to Korsakoff's syndrome predominantly affects the declarative memory, leaving non-declarative memory that is often procedural in nature relatively intact. The disproportionate severity in anterograde episodic memory processes in contrast to other cognitive processes is what differentiates Korsakoff syndrome from other conditions such as alcohol-related dementia. Evidence for the preservation of certain memory processes in the presence of severe anterograde episodic memory serve as experimental paradigm to investigate the components of human memory.

There are three generalized categories in which amnesia could be acquired by a person. The three categories are head trauma (example: head injuries), traumatic events (example: seeing something devastating to the mind), or physical deficiencies (example: atrophy of the hippocampus). The majority of amnesia and related memory issues derive from the first two categories as these are more common and the third could be considered a sub category of the first.

- Head trauma is a very broad range as it deals with any kind of injury or active action toward the brain which might cause amnesia. Retrograde and anterograde amnesia are more often seen from events like this, an exact example of a cause of the two would be electroshock therapy, which would cause both briefly for the receiving patient.

- Traumatic events are more subjective. What is traumatic is dependent on what the person finds to be traumatic. Regardless, a traumatic event is an event where something so distressing occurs that the mind chooses to forget rather than deal with the stress. A common example of amnesia that is caused by traumatic events is dissociative amnesia, which occurs when the person forgets an event that has deeply disturbed them. An example would be a person forgetting a fatal and graphic car accident involving their loved ones.

- Physical deficiencies are different from head trauma, because physical deficiencies lean more toward passive physical issues.

Amongst specific causes of amnesia are the following:

- Electroconvulsive therapy in which seizures are electrically induced in patients for therapeutic effect can have acute effects including both retrograde and anterograde amnesia.

- Alcohol can both cause blackouts and have deleterious effects on memory formation.

Anterograde amnesia is a loss of the ability to create new memories after the event that caused the amnesia, leading to a partial or complete inability to recall the recent past, while long-term memories from before the event remain intact. This is in contrast to retrograde amnesia, where memories created prior to the event are lost while new memories can still be created. Both can occur together in the same patient. To a large degree, anterograde amnesia remains a mysterious ailment because the precise mechanism of storing memories is not yet well understood, although it is known that the regions involved are certain sites in the temporal cortex, especially in the hippocampus and nearby subcortical regions.

Amnesia is a deficit in memory caused by brain damage, disease, or psychological trauma. Amnesia can also be caused temporarily by the use of various sedatives and hypnotic drugs. The memory can be either wholly or partially lost due to the extent of damage that was caused. There are two main types of amnesia: retrograde amnesia and anterograde amnesia. Retrograde amnesia is the inability to retrieve information that was acquired before a particular date, usually the date of an accident or operation. In some cases the memory loss can extend back decades, while in others the person may lose only a few months of memory. Anterograde amnesia is the inability to transfer new information from the short-term store into the long-term store. People with this type of amnesia cannot remember things for long periods of time. These two types are not mutually exclusive; both can occur simultaneously.

Case studies also show that amnesia is typically associated with damage to the medial temporal lobe. In addition, specific areas of the hippocampus (the CA1 region) are involved with memory. Research has also shown that when areas of the diencephalon are damaged, amnesia can occur. Recent studies have shown a correlation between deficiency of RbAp48 protein and memory loss. Scientists were able to find that mice with damaged memory have a lower level of RbAp48 protein compared to normal, healthy mice. In people suffering with amnesia, the ability to recall "immediate information" is still retained, and they may still be able to form new memories. However, a severe reduction in the ability to learn new material and retrieve old information can be observed. Patients can learn new procedural knowledge. In addition, priming (both perceptual and conceptual) can assist amnesiacs in the learning of fresh non-declarative knowledge. Amnesic patients also retain substantial intellectual, linguistic, and social skill despite profound impairments in the ability to recall specific information encountered in prior learning episodes. The term is ; .

Post-traumatic amnesia (PTA) is a state of confusion that occurs immediately following a traumatic brain injury in which the injured person is disoriented and unable to remember events that occur after the injury. The person may be unable to state his or her name, where he or she is, and what time it is. When continuous memory returns, PTA is considered to have resolved. While PTA lasts, new events cannot be stored in the memory. About a third of patients with mild head injury are reported to have "islands of memory", in which the patient can recall only some events. During PTA, the patient's consciousness is "clouded". Because PTA involves confusion in addition to the memory loss typical of amnesia, the term "post-traumatic confusional state" has been proposed as an alternative.

There are two types of amnesia: retrograde amnesia (loss of memories that were formed shortly before the injury) and anterograde amnesia (problems with creating new memories after the injury has taken place). Both retrograde and anterograde forms may be referred to as PTA, or the term may be used to refer only to anterograde amnesia.

A common example in sports concussion is the quarterback who was able to conduct the complicated mental tasks of leading a football team after a concussion, but has no recollection the next day of the part of the game that took place after the injury. Retrograde amnesia sufferers may partially regain memory later, but memories are not regained with anterograde amnesia because they were not encoded properly.

The term "post-traumatic amnesia" was first used in 1940 in a paper by Symonds to refer to the period between the injury and the return of full, continuous memory, including any time during which the patient was unconscious.

Pathophysiology is the study of the changes to an individual's normal physical, biological, and/or mental functions as a result of disease, injury, or other damage. Currently, the pathophysiological mechanisms which produce post-traumatic amnesia are not completely known. The most common research strategy to clarify these mechanisms is the examination of the impaired functional capabilities of people with post-traumatic amnesia (PTA) after a traumatic brain injury.

Symptoms of a dissociative fugue include mild confusion, and once the fugue ends, possible depression, grief, shame and discomfort. People have also experienced a post-fugue anger.

Dissociative fugue, formerly fugue state or psychogenic fugue, is a dissociative disorder. It is a rare psychiatric disorder characterized by reversible amnesia for personal identity, including the memories, personality, and other identifying characteristics of individuality. The state can last days, months or longer. Dissociative fugue usually involves unplanned travel or wandering, and is sometimes accompanied by the establishment of a new identity. It is a facet of dissociative amnesia, according to the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5).

After recovery from fugue, previous memories usually return intact. Because of this, there is not normally any treatment necessary for people who have been in fugue states. Additionally, an episode of fugue is not characterized as attributable to a psychiatric disorder if it can be related to the ingestion of psychotropic substances, to physical trauma, to a general medical condition, or to dissociative identity disorder, delirium, or dementia. Fugues are precipitated by a series of long-term traumatic episodes. It is most commonly associated with childhood victims of sexual abuse who learn over time to dissociate memory of the abuse (dissociative amnesia).

Normal aging, although not responsible for causing memory disorders, is associated with a decline in cognitive and neural systems including memory (long-term and working memory). Many factors such as genetics and neural degeneration have a part in causing memory disorders. In order to diagnose Alzheimer's disease and dementia early, researchers are trying to find biological markers that can predict these diseases in younger adults. One such marker is a beta-amyloid deposit which is a protein that deposits on the brain as we age. Although 20-33% of healthy elderly adults have these deposits, they are increased in elderly with diagnosed Alzheimer's disease and dementia.

Additionally, traumatic brain injury, TBI, is increasingly being linked as a factor in early-onset Alzheimer's disease.

One study examined dementia severity in elderly schizophrenic patients diagnosed with Alzheimer's disease and dementia versus elderly schizophrenic patients without any neurodegenerative disorders. In most cases, if schizophrenia is diagnosed, Alzheimer's disease or some form of dementia in varying levels of severity is also diagnosed. It was found that increased hippocampal neurofibrillary tangles and higher neuritic plaque density (in the superior temporal gyrus, orbitofrontal gyrus, and the inferior parietal cortex) were associated with increased severity of dementia. Along with these biological factors, when the patient also had the apolipoprotein E (ApoE4) allele (a known genetic risk factor for Alzheimer's disease), the neuritic plaques increased although the hippocampal neurofibrillary tangles did not. It showed an increased genetic susceptibility to more severe dementia with Alzheimer's disease than without the genetic marker.

As seen in the examples above, although memory does degenerate with age, it is not always classified as a memory disorder. The difference in memory between normal aging and a memory disorder is the amount of beta-amyloid deposits, hippocampal neurofibrillary tangles, or neuritic plaques in the cortex. If there is an increased amount, memory connections become blocked, memory functions decrease much more than what is normal for that age and a memory disorder is diagnosed.

The cholinergic hypothesis of geriatric memory dysfunction is an older hypothesis that was considered before beta-amyloid deposits, neurofibrillary tangles, or neuritic plaques. It states that by blocking the cholinergic mechanisms in control subjects you can examine the relationship between cholinergic dysfunction and normal aging and memory disorders because this system when dysfunctional creates memory deficits.

The fact that gastrointestinal surgery can lead to the development of WKS was demonstrated in a study that was completed on three patients who recently undergone a gastrectomy. These patients had developed WKS but were not alcoholics and had never suffered from dietary deprivation. WKS developed between 2 and 20 years after the surgery. There were small dietary changes that contributed to the development of WKS but overall the lack of absorption of thiamine from the gastrointestinal tract was the cause. Therefore, it must be ensured that patients who have undergone gastrectomy have a proper education on dietary habits, and carefully monitor their thiamine intake. Additionally, an early diagnosis of WKS, should it develop, is very important.

The most effective method of preventing Korsakoff's syndrome is to avoid B vitamin/thiamine deficiency. In Western nations, the most common causes of such a deficiency are alcoholism and eating disorders. Because these are behavioral-induced causes, Korsakoff's syndrome is essentially considered a preventable disease. Thus, fortifying foods with thiamine, or requiring companies that sell alcoholic beverages to supplement them with B vitamins in general or thiamine in particular, could avert many cases of Korsakoff's Syndrome.

Internationally, the prevalence rates of WKS are relatively standard, being anywhere between zero and two percent. Despite this, specific sub-populations seem to have higher prevalence rates including people who are homeless, older individuals (especially those living alone or in isolation), and psychiatric inpatients. Additionally, studies show that prevalence is not connected to alcohol consumption per capita. For example, in France, a country that is well known for its consumption and production of wine, prevalence was only 0.4% in 1994, while Australia had a prevalence of 2.8%.