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.

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.

Treatment for confabulation is somewhat dependent on the cause or source, if identifiable. For example, treatment of Wernicke–Korsakoff syndrome involves large doses of vitamin B in order to reverse the thiamine deficiency. If there is no known physiological cause, more general cognitive techniques may be used to treat confabulation. A case study published in 2000 showed that Self-Monitoring Training (SMT) reduced delusional confabulations. Furthermore, improvements were maintained at a three-month follow-up and were found to generalize to everyday settings. Although this treatment seems promising, more rigorous research is necessary to determine the efficacy of SMT in the general confabulation population.

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.

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.

Source amnesia is the inability to remember where, when or how previously learned information has been acquired, while retaining the factual knowledge. This branch of amnesia is associated with the malfunctioning of one's explicit memory. It is likely that the disconnect between having the knowledge and remembering the context in which the knowledge was acquired is due to a dissociation between semantic and episodic memory – an individual retains the semantic knowledge (the fact), but lacks the episodic knowledge to indicate the context in which the knowledge was gained.

Memory representations reflect the encoding processes during acquisition. Different types of acquisition processes (e.g.: reading, thinking, listening) and different types of events (e.g.: newspaper, thoughts, conversation) will produce mental depictions that perceptually differ from one another in the brain, making it harder to retrieve where information was learned when placed in a different context of retrieval. Source monitoring involves a systematic process of slow and deliberate thought of where information was originally learned. Source monitoring can be improved by using more retrieval cues, discovering and noting relations and extended reasoning.

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.

In psychiatry, confabulation (verb: confabulate) is a disturbance of memory, defined as the production of fabricated, distorted, or misinterpreted memories about oneself or the world, without the conscious intention to deceive. People who confabulate present incorrect memories ranging from "subtle alterations to bizarre fabrications", and are generally very confident about their recollections, despite contradictory evidence.

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.

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.

Memory distrust syndrome is a condition coined by Gísli Guðjónsson and James MacKeith in 1982, in which an individual doubts the accuracy of their memory concerning the content and context of events of which they have experienced. Since the individual does not trust their own memory, they will commonly depend on outside sources of information rather than using their ability for recollection. Some believe that this may be a defense or coping mechanism to a preexisting faulty memory state such as Alzheimer's disease, amnesia, or possibly dementia.

The condition is generally considered to be related to source amnesia, which involves the inability to recall the basis for factual knowledge. The main difference between the two is that source amnesia is a lack of knowing the basis of knowledge, whereas memory distrust syndrome is a lack of believing the knowledge that exists. The fact that an individual lacks the trust in their own memory implies that the individual would have a reason or belief that would prevent them from the trust that most of us have in our recollections. Cases concerning memory distrust syndrome have led to documented false confessions in court cases.

Treatment for topographical disorientation has been achieved through a case by case basis. Prognosis is largely dependent on the organic cause. Neuropsychological assessment followed by an assessment of unaffected cognitive abilities can be employed in therapy. Treatment for recovering navigational skills require strengthening unaffected navigational strategies to bypass defective ones.

A false memory is the psychological phenomenon where a person recalls something that did not happen. False memory is often considered in legal cases regarding childhood sexual abuse. This phenomenon was initially investigated by psychological pioneers Pierre Janet and Sigmund Freud. Freud wrote "The Aetiology of Hysteria", where he discussed repressed memories of childhood sexual trauma in their relation to hysteria. Elizabeth Loftus has, since her debuting research project in 1974, been a lead researcher in memory recovery and false memories. False memory syndrome recognizes false memory as a prevalent part of one's life in which it affects the person's mentality and day-to-day life. False memory syndrome differs from false memory in that the syndrome is heavily influential in the orientation of a person's life, while false memory can occur without this significant effect. The syndrome takes effect because the person believes the influential memory to be true. However, its research is controversial and the syndrome is excluded from identification as a mental disorder and, therefore, is also excluded from the "Diagnostic and Statistical Manual of Mental Disorders". False memory is an important part of psychological research because of the ties it has to a large number of mental disorders, such as PTSD.

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 ; .

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.

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.

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.

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.

False memory syndrome (FMS) describes a condition in which a person's identity and relationships are affected by memories that are factually incorrect but that they strongly believe. Peter J. Freyd originated the term, which the False Memory Syndrome Foundation (FMSF) subsequently popularized. The term is not recognized as a psychiatric illness in any of the medical manuals, such as the ICD-10 or the DSM-5; however, the principle that memories can be altered by outside influences is overwhelmingly accepted by scientists.

False memories may be the result of recovered memory therapy, a term also defined by the FMSF in the early 1990s, which describes a range of therapy methods that are prone to creating confabulations. Some of the influential figures in the genesis of the theory are forensic psychologist Ralph Underwager, psychologist Elizabeth Loftus, and sociologist Richard Ofshe.

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.

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.

False memory syndrome is a condition in which a person's identity and interpersonal relationships center on a memory of a traumatic experience that is objectively false but that the person strongly believes occurred.

The FMS concept is controversial, and the Diagnostic and Statistical Manual of Mental Disorders does not include it. Paul R. McHugh, member of the FMSF, stated that the term was not adopted into the fourth version of the manual due to the pertinent committee being headed by believers in recovered memory.

If a child experienced abuse, it is not typical for them to disclose the details of the event when confronted in an open-ended manner. Trying to indirectly prompt a memory recall can lead to the conflict of source attribution, as if repeatedly questioned the child may try to recall a memory to satisfy a question. The stress being put on the child can make recovering an accurate memory more difficult. Some people hypothesise that as the child continuously attempts to remember a memory, they are building a larger file of sources that the memory could be derived from, potentially including sources other than genuine memories. Children that have never been abused that undergo similar response-eliciting techniques can disclose events that never occurred. If one concludes that the child's recalled memory is false, it is a type I error. Assuming the child did not recall an existing memory, it is a type II error.

One of children's most notable setbacks in memory recall is source misattribution. Source misattribution is the flaw in deciphering between potential origins of a memory. The source could come from an actual occurring perception, or it can come from an induced and imagined event. Younger children, preschoolers in particular, find it more difficult to discriminate between the two. Lindsay & Johnson (1987) concluded that even children approaching adolescence struggle with this, as well as recalling an existent memory as a witness. Children are significantly more likely to confuse a source between being invented or existent.