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.

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.

Two types of confabulation are often distinguished:

- Provoked (momentary, or secondary) confabulations represent a normal response to a faulty memory, are common in both amnesia and dementia, and can become apparent during memory tests.

- Spontaneous (or primary) confabulations do not occur in response to a cue and seem to be involuntary. They are relatively rare, more common in cases of dementia, and may result from the interaction between frontal lobe pathology and organic amnesia.

Another distinction is that between:

- Verbal confabulations, spoken false memories are more common, and

- Behavioral confabulations, occur when an individual acts on their false memories.

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.

Psychogenic amnesia, also known as dissociative amnesia, is a memory disorder characterized by sudden retrograde episodic memory loss, said to occur for a period of time ranging from hours to years. More recently, "dissociative amnesia" has been defined as a dissociative disorder "characterized by retrospectively reported memory gaps. These gaps involve an inability to recall personal information, usually of a traumatic or stressful nature." In a change from the DSM-IV to the DSM-5, dissociative fugue is now subsumed under dissociative amnesia.

The atypical clinical syndrome of the memory disorder (as opposed to organic amnesia) is that a person with psychogenic amnesia is profoundly unable to remember personal information about themselves; there is a lack of conscious self-knowledge which affects even simple self-knowledge, such as who they are. Psychogenic amnesia is distinguished from organic amnesia in that it is supposed to result from a nonorganic cause; no structural brain damage or brain lesion should be evident but some form of psychological stress should precipitate the amnesia, however psychogenic amnesia as a memory disorder is controversial.

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.

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.

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.

Repressed memories are memories that have been unconsciously blocked due to the memory being associated with a high level of stress or trauma. The theory postulates that even though the individual cannot recall the memory, it may still be affecting them consciously, and that these memories can emerge later into the consciousness. Ideas on repressed memory hiding trauma from awareness were an important part of Sigmund Freud's early work on psychoanalysis. He later took a different view.

The existence of repressed memories is an extremely controversial topic in psychology; although some studies have concluded that it can occur in a varying but generally small percentage of victims of trauma, many other studies dispute its existence entirely. Some psychologists support the theory of repressed memories and claim that repressed memories can be recovered through therapy, but most psychologists argue that this is in fact rather a process through which false memories are created by blending actual memories and outside influences. One study concluded that repressed memories were a cultural symptom due to the lack of written proof of their existence before the nineteenth century, but its results were disputed by some psychologists, and the lack of written proof was eventually partially disproven.

According to the American Psychological Association, it is not possible to distinguish repressed memories from false ones without corroborating evidence. The term repressed memory is sometimes compared to the term dissociative amnesia, which is defined in the DSM-V as an “inability to recall autobiographical information. This amnesia may be localized (i.e., an event or period of time), selective (i.e., a specific aspect of an event), or generalized (i.e., identity and life history).”

According to the Mayo Clinic, amnesia refers to any instance in which memories stored in the long-term memory are completely or partially forgotten, usually due to brain injury.

According to proponents of the existence of repressed memories, such memories can be recovered years or decades after the event, most often spontaneously, triggered by a particular smell, taste, or other identifier related to the lost memory, or via suggestion during psychotherapy.

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.

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.

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.

People with anterograde amnesic syndromes may present with widely varying degrees of forgetfulness. Some with severe cases have a combined form of anterograde and retrograde amnesia, sometimes called global amnesia.

In the case of drug-induced amnesia, it may be short-lived and patients can recover from it. In the other case, which has been studied extensively since the early 1970s, patients often have permanent damage, although some recovery is possible, depending on the nature of the pathophysiology. Usually, some capacity for learning remains, although it may be very elementary. In cases of pure anterograde amnesia, patients have recollections of events prior to the injury, but cannot recall day-to-day information or new facts presented to them after the injury occurred.

In most cases of anterograde amnesia, patients lose declarative memory, or the recollection of facts, but they retain nondeclarative memory, often called procedural memory. For instance, they are able to remember and in some cases learn how to do things such as talking on the phone or riding a bicycle, but they may not remember what they had eaten earlier that day for lunch. One extensively studied anterograde amnesiac patient, codenamed H.M., demonstrated that despite his amnesia preventing him from learning new declarative information, procedural memory consolidation was still possible, albeit severely reduced in power. He, along with other patients with anterograde amnesia, were given the same maze to complete day after day. Despite having no memory of having completed the maze the day before, unconscious practice of completing the same maze over and over reduced the amount of time needed to complete it in subsequent trials. From these results, Corkin et al. concluded despite having no declarative memory (i.e. no conscious memory of completing the maze exists), the patients still had a working procedural memory (learning done unconsciously through practice). This supports the notion that declarative and procedural memory are consolidated in different areas of the brain. In addition, patients have a diminished ability to remember the temporal context in which objects were presented. Certain authors claim the deficit in temporal context memory is more significant than the deficit in semantic learning ability (described below).

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 ; .

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.

Retrograde amnesia (RA) is a loss of memory-access to events that occurred, or information that was learned, before an injury or the onset of a disease. It tends to negatively affect episodic, autobiographical, and declarative memory while usually keeping procedural memory intact with no difficulty for learning new knowledge. RA can be temporally graded or more permanent based on the severity of its cause and is usually consistent with Ribot's Law: where subjects are more likely to lose memories closer to the traumatic incident than more remote memories. The type of information that is forgotten can be very specific, like a single event, or more general, resembling generic amnesia. It is not to be confused with anterograde amnesia, which deals with the inability to form new memories following the onset of an injury or disease.

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.

A doctor may suspect dissociative fugue when people seem confused about their identity or are puzzled about their past or when confrontations challenge their new identity or absence of one. The doctor carefully reviews symptoms and does a physical examination to exclude physical disorders that may contribute to or cause memory loss. A psychological examination is also done.

Sometimes dissociative fugue cannot be diagnosed until people abruptly return to their pre-fugue identity and are distressed to find themselves in unfamiliar circumstances. The diagnosis is usually made retroactively when a doctor reviews the history and collects information that documents the circumstances before people left home, the travel itself, and the establishment of an alternative life.

Functional amnesia can also be situation specific, varying from all forms and variations of traumas or generally violent experiences, with the person experiencing severe memory loss for a particular trauma. Committing homicide; experiencing or committing a violent crime such as rape or torture; experiencing combat violence; attempting suicide; and being in automobile accidents and natural disasters have all induced cases of situation-specific amnesia (Arrigo & Pezdek, 1997; Kopelman, 2002a). As Kopelman (2002a) notes, however, care must be exercised in interpreting cases of psychogenic amnesia when there are compelling motives to feign memory deficits for legal or financial reasons. However, although some fraction of psychogenic amnesia cases can be explained in this fashion, it is generally acknowledged that true cases are not uncommon. Both global and situationally specific amnesia are often distinguished from the organic amnesic syndrome, in that the capacity to store new memories and experiences remains intact. Given the very delicate and often times dramatic nature of memory loss in these such cases, there usually is a concerted effort to help the person recover their identity and history. This will allow the subject to sometimes be recovered spontaneously when particular cures are encountered.

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.

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.

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.

Individuals with frontal lobe damage have deficits in temporal context memory; source memory can also exhibit deficits in those with frontal lobe damage. It appears that those with frontal lobe damage have difficulties with recency and other temporal judgements (e.g., placing events in the order they occurred), and as such they are unable to properly attribute their knowledge to appropriate sources (i.e., suffer source amnesia). Those individuals with frontal lobe damage have normal recall of facts, but they make significantly more errors in source memory than control subjects, with these effects becoming apparent as shortly as 5 minutes after the learning experience. Individuals with frontal lobe damage often mistakenly attribute the knowledge they have to some other source (e.g., they read it somewhere, saw it on TV, etc.) but rarely attribute it to having learned it over the course of the experiment. It appears that frontal lobe damage causes a disconnection between semantic and episodic memory – in that the individuals cannot associate the context in which they acquired the knowledge to the knowledge itself.

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.

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.

Individuals with hyperthymesia can recall almost every day of their lives in near perfect detail, as well as public events that hold some personal significance to them. Those affected describe their memories as uncontrollable associations; when they encounter a date, they "see" a vivid depiction of that day in their heads. Recollection occurs without hesitation or conscious effort.

It is important to draw a distinction between those with hyperthymesia and those with other forms of exceptional memory, who generally use mnemonic or similar rehearsal strategies to memorize long strings of subjective information. Memories recalled by hyperthymestic individuals tend to be personal, autobiographical accounts of both significant and mundane events in their lives. This extensive and highly unusual memory does not derive from the use of mnemonic strategies; it is encoded involuntarily and retrieved automatically. Despite being able to remember the day of the week on which a particular date fell, hyperthymestics are not calendrical calculators like some people with autism or savant syndrome. Rather, hyperthymestic recall tends to be constrained to a person's lifetime and is believed to be a subconscious process.

Although hyperthymestics are not necessarily autistic, and likewise savants do not necessarily memorize autobiographical information, certain similarities exist between the two conditions. Like autistic savants, some individuals with hyperthymesia may also have an unusual and obsessive interest in dates. Russian psychologist Alexander Luria documented the famous case of mnemonist Solomon Shereshevsky, who was quite different from the first documented hyperthymestic known as AJ (real name Jill Price) in that Shereshevskii could memorize virtually unlimited amounts of information deliberately, while AJ could not – she could only remember autobiographical information (and events she had personally seen on the news or read about). In fact, she was not very good at memorizing anything at all, according to the study published in "Neurocase". Hyperthymestic individuals appear to have poorer than average memory for arbitrary information. Another striking parallel drawn between the two cases was that Shereshevsky exemplified an interesting case of synesthesia and it has been suggested that superior autobiographical memory is intimately tied to time-space synaesthesia.