Many forms of amnesia fix themselves without being treated. However, there are a few ways to cope with memory loss if that is not the case. One of these ways is cognitive or occupational therapy. In therapy, amnesiacs will develop the memory skills they have and try to regain some they have lost by finding which techniques help retrieve memories or create new retrieval paths. This may also include strategies for organizing information to remember it more easily and for improving understanding of lengthy conversation.

Another coping mechanism is taking advantage of technological assistance, such as a personal digital device to keep track of day-to-day tasks. Reminders can be set up for appointments, when to take medications, birthdays and other important events. Many pictures can also be stored to help amnesiacs remember names of friends, family and co-workers. Notebooks, wall calendars, pill reminders and photographs of people and places are low-tech memory aids that can help as well.

While there are no medications available to treat amnesia, underlying medical conditions can be treated to improve memory. Such conditions include but are not limited to low thyroid function, liver or kidney disease, stroke, depression, bipolar disorder and blood clots in the brain. Wernicke–Korsakoff syndrome involves a lack of thiamin and replacing this vitamin by consuming thiamin-rich foods such as whole-grain cereals, legumes (beans and lentils), nuts, lean pork, and yeast. Treating alcoholism and preventing alcohol and illicit drug use can prevent further damage, but in most cases will not recover lost memory.

Although improvements occur when patients receive certain treatments, there is still no actual cure remedy for amnesia so far. To what extent the patient recovers and how long the amnesia will continue depends on the type and severity of the lesion.

Because psychogenic amnesia is defined by its lack of physical damage to the brain, treatment by physical methods is difficult. Nonetheless, distinguishing between organic and dissociative memory loss has been described as an essential first-step in effective treatments. Treatments in the past have attempted to alleve psychogenic amnesia by treating the mind itself, as guided by theories which range from notions such as 'betrayal theory' to account for memory loss attributed to protracted abuse by caregivers to the amnesia as a form of self-punishment in a Freudian sense, with the obliteration of personal identity as an alternative to suicide.

Treatment attempts often have revolved around trying to discover what traumatic event had caused the amnesia, and drugs such as intravenously administered barbiturates (often thought of as 'truth serum') were popular as treatment for psychogenic amnesia during World War II; benzodiazepines may have been substituted later. 'Truth serum' drugs were thought to work by making a painful memory more tolerable when expressed through relieving the strength of an emotion attached to a memory. Under the influence of these 'truth' drugs the patient would more readily talk about what had occurred to them. However, information elicited from patients under the influence of drugs such as barbiturates would be a mixture of truth and fantasy, and was thus not regarded as scientific in gathering accurate evidence for past events. Often treatment was aimed at treating the patient as a whole, and probably varied in practice in different places. Hypnosis was also popular as a means for gaining information from people about their past experiences, but like 'truth' drugs really only served to lower the threshold of suggestibility so that the patient would speak easily but not necessarily truthfully. If no motive for the amnesia was immediately apparent, deeper motives were usually sought by questioning the patient more intensely, often in conjunction with hypnosis and 'truth' drugs. In many cases, however, patients were found to spontaneously recover from their amnesia on their own accord so no treatment was required.

Approaches used to treat those who suffer from anterograde amnesia often use interventions which focus on compensatory techniques, such as beepers, written notes, diaries or through intensive training programs involving the active participation of the individual concerned, along with their supporting network of family and friends.

In this perspective, environmental adaptation techniques are used, such as the compensatory technique education to training (exercise), organizational strategies, visual imagery and verbal labeling. In addition, other techniques are also used in rehabilitation, such as implicit tasks, speech and mnemotechnic methods.

So far, it has been proven that education techniques of compensatory strategies for memory disorders are effective in individuals with minor traumatic brain injuries. In moderately or severely injured individuals, effective interventions are those appealing to external aids, such as reminders in order to facilitate particular knowledge or skill acquisition. Reality orientation techniques are also considered; Their purpose is to enhance orientation using stimulation and repetition of the basic orientation information. These techniques are regularly applied in populations of patients primarily presenting with dementia and head-injured patients.

When someone is suffering from RA, their memory cannot be recovered from simply being told personal experiences and their identity. This is called reminder effect or reminder treatment. The reminder effect consists of re-exposing the patient to past personal information, which cannot reverse RA. Thus, reminding the patient details of their life has no scientific bearings on recovering memory. Fortunately, memory can be and usually is recovered due to spontaneous recovery and plasticity.

Amnesia can result from a side-effect of prescription or non-prescription drugs. Both substance use and alcohol can cause both long-term and short-term memory loss, resulting in blackouts.

The most commonly used group of prescription drugs which can produce amnesia are benzodiazepines, especially if combined with alcohol, however, in limited quantities, triazolam (Halcion) is not associated with amnesia or memory impairment.

Clinically induced RA has been achieved using different forms of electrical induction.

- Electroconvulsive therapy (ECT), used as a depression therapy, can cause impairments in memory. Tests show that information of days and weeks before the ECT can be permanently lost. The results of this study also show that severity of RA is more extreme in cases of bilateral ECT rather than unilateral ECT. Impairments can also be more intense if ECT is administered repetitively (sine wave simulation) as opposed to a single pulse (brief-pulse stimulation).

- Electroconvulsive shock (ECS): The research in this field has been advanced by using animals as subjects. Researchers induce RA in rats, for example, by giving daily ECS treatments. This is done to further understand RA.

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 ; .

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.

One subsequent human study found no effects of vasopressin on memory. The nonsignificant results were attributed to the study's many potential flaws, particularly its small sample size, the inability of vasopressin to penetrate the blood brain barrier when administered as a nasal spray, inadequate dosing and differences in severity of head injury between the samples. However, Eames et al. (1999) found statistically significant improvements on several tests of memory with the use of a vasopressin nasal spray, with no reported ill effects. Although the degree of improvement was mild, and it could be attributed to numerous other factors of the rehabilitative program, the lack of any ill effects suggests that vasopressin is, at the least, a possible enhancement for a treatment regimen.

Diaschisis, as mentioned earlier, has been linked to the mechanism of PTA. The noradrenergic systems may play a role in diaschisis. Norepinephrine, also known as noradrenalin, is a catecholamine neurotransmitter. Administering a norepinephrine receptor agonist (a substance that initiates a cell response when it binds with a receptor) to patients promoted the recovery of memory and many other cognitive functions after a traumatic brain injury. Conversely, the administration of norpinephrine antagonists slowed recovery, and could lead to the reinstatement of deficits when administered after recovery. Noradrenergic antagonists were not prescribed for the purposes of slowing the recovery of memory. Rather, these findings are based on the effects of other commonly prescribed drugs that happen to block noradrenergic receptors. The alpha-1 adrenergic receptor is specifically implicated. Although it has not yet been thoroughly investigated, there is potential for stimulants, which promote catecholamine release, to be an effective treatment in the early stages of recovery from brain trauma, and these positive effects could reduce the symptoms of PTA.

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.

Source amnesia is not a rare phenomenon – everybody experiences it on a near daily basis as, for much of our knowledge, it is important to remember the knowledge itself, rather than its source. However, there are extreme examples of source amnesia caused by a variety of factors.

Amnesia is desirable during surgery, since a general anaesthetic should also give the person amnesia for the operation. Sedatives such as benzodiazepines, which are commonly used for anxiety disorders, can reduce the encoding of new memories, particularly in high doses (for example, prior to surgery in order for a person not to recall the surgery). Amnesiac drugs can be used to induce a coma for a child breathing using mechanical ventilation, or to help reduce intracranial pressure after head trauma.

Researchers are currently experimenting with drugs which induce amnesia in order to improve understanding of human memory, and develop better drugs to treat psychiatric disorders and memory related disorders. People with Alzheimer's disease and other forms of dementia are likely to benefit. By understanding the ways in which amnesia-inducing drugs interact with the brain, researchers hope to better understand the ways in which neurotransmitters aid in the formation of memory. By stimulating rather than depressing these neurotransmitters, memory may improve.

The use of a drug to erase traumatic or unwanted memories used to be referred to as "science fiction." Holmes et al. (2010) commented that the media misrepresented two recent studies as research on "erasing" traumatic memories, but showed the fear response associated with stressful memory could be greatly reduced whilst the factual memory of the trauma remained intact. Similarly, Brunet et al. (2008) found that the people with chronic Posttraumatic Stress Disorder who were treated with propranolol for a single day had a reduced response to existing trauma while retaining memory of the trauma. In the process of remembering, the memory needs to be restored in the brain. By introducing an amnesia-inducing drug during this process, the memory can be disrupted. While the memory remains intact, the emotional reaction is dampened, making the memory less overwhelming. Researchers believe this drug will help patients with post-traumatic stress disorder be able to better process the trauma without reliving the trauma emotionally. This has raised legal/ethical concerns should drugs be found to have altered the memory of traumatic events that occur in victims of crimes (e.g. rape), and whether it is therapeutically desirable to do so.

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.

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.

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.

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.

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.

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.

Memories "can" be accurate, but they are not "always" accurate. For example, eyewitness testimony even of relatively recent dramatic events is notoriously unreliable. Misremembering may result from confusion of memories of perceived and imagined events, as there may be overlap between features of the stored information comprising memories for perceived and imagined events. Memories of events are always a mix of factual traces of sensory information overlaid with emotions, mingled with interpretation and "filled in" with imaginings. Thus there is always skepticism about how valid a memory is as evidence of factual detail.

In one study where victims of documented child abuse were reinterviewed many years later as adults, 38% of the women denied any memory of the abuse.

Arguments against the existence of "traumatic amnesia" note that various manipulations can be used to implant false memories (sometimes called "pseudomemories"). These can be quite compelling for those who develop them, and can include details that make them seem credible to others. A classic experiment in memory research, conducted by Elizabeth Loftus, became widely known as "Lost in the Mall"; in this, subjects were given a booklet containing three accounts of real childhood events written by family members and a fourth account of a wholly fictitious event of being lost in a shopping mall. A quarter of the subjects reported remembering the fictitious event, and elaborated on it with extensive circumstantial detail. This experiment inspired many others, and in one of these, Porter et al. could convince about half of his subjects that they had survived a vicious animal attack in childhood.

Such experimental studies have been criticized in particular about whether the findings are really relevant to trauma memories and psychotherapeutic situations. Nevertheless, these studies prompted public and professional concern about recovered memory therapy for past sexual abuse. When memories are "recovered" after long periods of amnesia, particularly when extraordinary means were used to secure the recovery of memory, it is now widely (but not universally) accepted that the memories are quite likely to be false, i.e. of incidents that had not occurred. It is thus recognised by professional organizations that a risk of implanting false memories is associated with some similar types of therapy. The "American Psychiatric Association" advises: "...most leaders in the field agree that although it is a rare occurrence, a memory of early childhood abuse that has been forgotten can be remembered later. However, these leaders also agree that it is possible to construct convincing pseudomemories for events that never occurred.

Nevertheless, many therapists believe in the authenticity of the recovered memories that they hear from their clients. In a non-random study by Loftus and Herzog (1991) with 16 clinicians, 13 (81%) said that they invariably believed their clients. The most common basis for this belief was the patient’s symptomology (low self-esteem, sexual dysfunction, self-destructive behaviour) or body memories (voice frozen etc.).

The mechanism(s) by which both of these phenomena happen are not well understood and, at this point it is impossible, without other corroborative evidence, to distinguish a true memory from a false one." Sheflin and Brown state that a total of 25 studies on amnesia for child sexual abuse exist and that they demonstrate amnesia in their study subpopulations. However, an editorial in the "British Medical Journal" states on the Sheflin and Brown study that "on critical examination, the scientific evidence for repression crumbles."

Obviously, not all therapists agree that false memories are a major risk of psychotherapy and they argue that this idea overstates the data and is untested.

Both true and false "memories" can be recovered using memory work techniques, but there is no evidence that reliable discriminations can be made between them. Some believe that memories "recovered" under hypnosis are particularly likely to be false.

According to The Council on Scientific Affairs for the American Medical Association, recollections obtained during hypnosis can involve confabulations and pseudomemories and appear to be less reliable than nonhypnotic recall.

Brown et al. estimate that 3 to 5% of laboratory subjects are vulnerable to post-event misinformation suggestions. They state that 5–8% of the general population is the range of high-hypnotizability. Twenty-five percent of those in this range are vulnerable to suggestion of pseudomemories for peripheral details, which can rise to 80% with a combination of other social influence factors. They conclude that the rates of memory errors run 0–5% in adult studies, 3–5% in children's studies and that the rates of false allegations of child abuse allegations run 4–8% in the general population.

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.

It was once assumed that anyone suffering from Korsakoff's syndrome would eventually need full-time care. This is still often the case, but rehabilitation can help regain some, albeit often limited, level of independence. Treatment involves the replacement or supplementation of thiamine by intravenous (IV) or intramuscular (IM) injection, together with proper nutrition and hydration. However, the amnesia and brain damage caused by the disease does not always respond to thiamine replacement therapy. In some cases, drug therapy is recommended. Treatment of the patient typically requires taking thiamine orally for 3 to 12 months, though only about 20 percent of cases are reversible. If treatment is successful, improvement will become apparent within two years, although recovery is slow and often incomplete.

As an immediate form of treatment, a pairing of IV or IM thiamine with a high concentration of B-complex vitamins can be administered three times daily for period of 2–3 days. In most cases, an effective response from patients will be observed. A dose of 1 gram of thiamine can also be administered to achieve a clinical response. In patients who are seriously malnourished, the sudden availability of glucose without proper bodily levels of thiamine to metabolize is thought to cause damage to cells. Thus, the administration of thiamine along with an intravenous form of glucose is often good practice.

Treatment for the memory aspect of Korsakoff's syndrome can also include domain-specific learning, which when used for rehabilitation is called the method of vanishing cues. Such treatments aim to use patients' intact memory processes as the basis for rehabilitation. Patients who used the method of vanishing cues in therapy were found to learn and retain information more easily.

People diagnosed with Korsakoff's are reported to have a normal life expectancy, presuming that they abstain from alcohol and follow a balanced diet. Empirical research has suggested that good health practices have beneficial effects in Korsakoff's syndrome.

As described, Korsakoff 's syndrome usually follows or accompanies Wernicke's encephalopathy. If treated quickly, it may be possible to prevent the development of Korsakoff's syndrome with thiamine treatments. This treatment is not guaranteed to be effective and the thiamine needs to be administered adequately in both dose and duration. A study on Wernicke-Korsakoff's syndrome showed that with consistent thiamine treatment there were noticeable improvements in mental status after only 2–3 weeks of therapy. Thus, there is hope that with treatment Wernicke's encephalopathy will not necessarily progress to WKS.

In order to reduce the risk of developing WKS it is important to limit the intake of alcohol or drink in order to ensure that proper nutrition needs are met. A healthy diet is imperative for proper nutrition which, in combination with thiamine supplements, may reduce the chance of developing WKS. This prevention method may specifically help heavy drinkers who refuse to or are unable to quit.

The DSM-IV-TR states that the fugue may have a duration from days to months, and recovery is usually rapid. However, some cases may be refractory. An individual usually has only one episode.