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.

As previously mentioned, RA can affect people's memories in different degrees, but testing is required to help determine if someone is experiencing RA. Several tests exist, for example, testing for factual knowledge such as known public events. A problem with this form of testing is that people generally differ in their knowledge of such subjects. Other ways to test someone is via autobiographical knowledge using the Autobiographical Memory Interview (AMI), comprising names of relatives, personal information, and job history. This information could help determine if someone is experiencing RA and the degree of memory affected. However, due to the nature of the information being tested, it is often difficult to verify the accuracy of the memories being recalled, especially if they are from a distant past. Some researchers have found that the time interval after the head injury occurred did not seem to matter. The effect of the memory loss was the same no matter how long it had been after from the injury.

Brain abnormalities can be measured using magnetic resonance imaging (MRI), computed tomography scan (CT) and electroencephalography (EEG), which can provide detailed information about specific brain structures. In many cases, an autopsy helps identify the exact brain region affected and the extent of the damage that caused RA once the patient has died.

There are some aspects essential to the patient that remain unaffected by RA. In many patients, their personality remains the same. Also, semantic memory, that is general knowledge about the world, is usually unaffected. However, episodic memory, which refers to one's life experiences, is impaired.

Another real life problem with RA is malingering, which is conceived as the rational output of a neurologically normal brain aiming at the surreptitious achievement of a well identified gain. Since it is common for people who have committed a crime to report having RA for that specific event in order to avoid their punishment, the legal system has pushed for the creation of a standardized test of amnesia. However, since most cases differ in onset, duration, and content forgotten, this task has shown to be a rather complex one.

Functional assessment of brain activity can be assessed for psychogenic amnesia using imaging techniques such as fMRI, PET and EEG, in accordance with clinical data. Some research has suggested that organic and psychogenic amnesia to some extent share the involvement of the same structures of the temporo-frontal region in the brain. It has been suggested that deficits in episodic memory may be attributable to dysfunction in the limbic system, while self-identity deficits have been suggested as attributable to functional changes related to the posterior parietal cortex. To reiterate however, care must be taken when attempting to define causation as only "ad hoc" reasoning about the aetiology of psychogenic amnesia is possible, which means cause and consequence can be infeasible to untangle.

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.

The Wisconsin Card Sorting Test is widely used in clinical settings to test for cognitive impairments, such as frontal lobe disorder which has been associated with source amnesia.

- Procedure:

The visuo-spatial component of this test is devised of two sets of 12 identical cards. The figures on the cards differ with respect to color, quantity, and shape. The participants are then given a pile of additional cards and are asked to match each one to one of the previous cards.

- Results:

Patients suffering from frontal lobe dysfunction and ultimately source amnesia, will have much greater difficulty finishing this task successfully through method of strategy.

The verbal fluency test is a widely and commonly used test to assess for frontal lobe dysfunction in patients.

- Procedure:

Participants are asked to generate words beginning with letters that had previously been introduced to them (e.g.: generate a word beginning with 'A' or 'R'). They are given three 1-min trials (one trial per letter). The goal is to say as many different words possible that begin with the given letter.

- Results:

The Verbal fluency test can assess for damage in the prefrontal lobes, which has been associated with patients suffering from source amnesia. Patients with frontal lobe disorder have trouble putting verbal items into a proper sequential order, monitor personal behaviors as well as a deficient judgment in recency. All of these behaviors are required for the proper recall of the source of a memory.

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 there is damage to just one side of the MTL, there is opportunity for normal functioning or near-normal function for memories. Neuroplasticity describes the ability of the cortex to remap when necessary. Remapping can occur in cases like the one above, and, with time, the patient can recover and become more skilled at remembering. A case report describing a patient who had two lobectomies – in the first, doctors removed part of her right MTL first because of seizures originating from the region, and later her left because she developed a tumor – demonstrates this. This case is unique because it is the only one in which both sides of the MTL were removed at different times. The authors observed that the patient was able to recover some ability to learn when she had only one MTL, but observed the deterioration of function when both sides of the MTL were afflicted. The reorganization of brain function for epileptic patients has not been investigated much, but imaging results show that it is likely.

Topographical disorientation is usually diagnosed with the use of a comprehensive battery of neuropsychological tests combined with a variety of orientation tasks performed by the participants in both virtual and real surroundings. Performance on certain tests can identify underlying neurological disorders and verify the disorientation as a selective impairment. Brain imaging is used to determine regions of brain damage, if any. Navigational skills can be assessed by tests pertaining to memory, visual-perceptual abilities, object recognition, mental rotation, imagery abilities, and spatial abilities. More direct testing of navigation involves asking the patient to describe a route, read a map, draw a map, follow a route, or point out landmarks.

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.

Confabulations can also be researched by using continuous recognition tasks. These tasks are often used in conjunction with confidence ratings. Generally, in a recognition task, participants are rapidly presented with pictures. Some of these pictures are shown once; others are shown multiple times. Participants press a key if they have seen the picture previously. Following a period of time, participants repeat the task. More errors on the second task, versus the first, are indicative of confusion, representing false memories.

Confabulations can also be detected using a free recall task, such as a self-narrative task. Participants are asked to recall stories (semantic or autobiographical) that are highly familiar to them. The stories recalled are encoded for errors that could be classified as distortions in memory. Distortions could include falsifying true story elements or including details from a completely different story. Errors such as these would be indicative of confabulations.

The Gudjonsson Compliance Scale is a self-report instrument that measures peoples' levels of compliance. It focuses on two types of behavior, namely eagerness to please others, and avoidance of conflicts. The scale consists of 20 items using

a true/false format. Examples are 'I give in easily to people when I am pressured' and 'I try hard to do what is expected of me'. After recoding items 17 to 19, a total GCS score varying from 0 to 20 can be obtained by summing the number of true responses, with higher scores indexing more compliant behavior.

PTA has been proposed to be the best measure of head trauma severity, but it may not be a reliable indicator of outcome.

However, PTA duration may be linked to the likelihood that psychiatric and behavioral problems will occur as consequences of TBI.

Classification systems for determining the severity of TBI may use duration of PTA alone or with other factors such as Glasgow Coma Scale (GCS) score and duration of loss of consciousness (LOC) to divide TBI into categories of mild, moderate, and severe. One common system using all three factors and one using PTA alone are shown in the tables at right. Duration of PTA usually correlates well with GCS and usually lasts about four times longer than unconsciousness.

PTA is considered a hallmark of concussion, and is used as a measure of predicting its severity, for example in concussion grading scales. It may be more reliable for determining severity of concussion than GCS because the latter may not be sensitive enough; concussion sufferers often quickly regain a GCS score of 15.

Longer periods of amnesia or loss of consciousness immediately after the injury may indicate longer recovery times from residual symptoms from concussion.

Increased duration of PTA is associated with a heightened risk for TBI complications such as post-traumatic epilepsy.

Before the development of the current tests for the assessment of post-traumatic amnesia (PTA), a retrospective method was used to determine the patient's condition, consisting of one or more interviews with the patient after the episode of PTA was judged to be over. The retrospective method, however, fails to account for the apparent lucidity of patients who are still experiencing substantial disorientation, or the finding that the recovery from post-traumatic amnesia is often characterized by the presence of "islands of memory" (short periods of clarity). A failure to take these facts into consideration may have biased retrospective methods towards underestimating the length and severity of an episode of PTA. Also, the retrospective method relies on retrospective memory, one's memory for past events, which is not very reliable in healthy individuals, and even less so in patients who have recently experienced a traumatic brain injury (TBI). Patients may also unconsciously or consciously bias their answers because they want to appear more healthy or more ill than they truly were, or because of poor insight. The retrospective method is also flawed because there is no standard measurement procedure. Although the retrospective method may provide useful subjective data, it is not a useful tool for measurement or categorization.

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 ; .

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.

The Gudjonsson suggestibility scale (GSS) is used to measure interrogative suggestibility. The GSS consists of a story that is read out loud by a test administer. Participants then have to answer 20 questions of which 15 are misleading and 5 are neutral and address factual details of the story. After participants have answered the questions, they receive negative feedback about their performance. They are asked to answer the questions one more time and to be more accurate this time. Thus, all questions are answered twice and in this way several GSS parameters can be calculated. First, yield 1 refers to the number of misleading questions that the participant accepts during the first round (range 0–15). Second, yield 2 refers to the number of misleading questions accepted during the second round (range 0–15). Third, shift refers to the number of changes that participants make in their answers after having received negative feedback (range 0–20). Finally, the total GSS score is the sum of yield 1 and shift, with higher scores reflecting higher levels of interrogative suggestibility (range 0–35).

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.

Diagnosis of Wernicke–Korsakoff syndrome is by clinical impression and can sometimes be confirmed by a formal neuropsychological assessment. Wernicke's encephalopathy typically presents with ataxia and nystagmus, and Korsakoff's psychosis with anterograde and retrograde amnesia and confabulation upon relevant lines of questioning.

Frequently, secondary to thiamine deficiency and subsequent cytotoxic edema in Wernicke's encephalopathy, patients will have marked degeneration of the mamillary bodies. Thiamine (vitamin B) is an essential coenzyme in carbohydrate metabolism and is also a regulator of osmotic gradient. Its deficiency may cause swelling of the intracellular space and local disruption of the blood-brain barrier. Brain tissue is very sensitive to changes in electrolytes and pressure and edema can be cytotoxic. In Wernicke's this occurs specifically in the mammillary bodies, medial thalami, tectal plate, and periaqueductal areas. Sufferers may also exhibit a dislike for sunlight and so may wish to stay indoors with the lights off. The mechanism of this degeneration is unknown, but it supports the current neurological theory that the mammillary bodies play a role in various "memory circuits" within the brain. An example of a memory circuit is the Papez circuit.

There have been assertions of a possible link between TGA and the use of statins (a class of drug used in treating cholesterol).

En bloc memory loss which is total, permanent, and irrecoverable can occur as an alcoholic "black out," usually lasting longer than an hour and up to 2–5 days.

Marijuana intoxication, Halogenated hydroxyquinolines such as Clioquinol, PDE inhibitors such as sildenafil, Digitalis and scopolamine intoxication, and general anaesthesia have been reported with TGA.

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.

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 existence of repressed memory recovery has not been accepted by mainstream psychology, nor unequivocally proven to exist, and some experts in the field of human memory feel that no credible scientific support exists for the notions of repressed/recovered memories. A survey revealed that whilst memory and cognition experts tend to be skeptical of repressed memory, clinicians are much more apt to believe that traumatic memory is often repressed. One research report states that a distinction should be made between spontaneously recovered memories and memories recovered during suggestions in therapy. A common criticism is that a recovered memory is tainted by, or a product of, the process of recovery or the suggestions used in that process.

The "Working Group on Investigation of Memories of Child Abuse" of the American Psychological Association presented findings mirroring those of the other professional organizations. The Working Group made five key conclusions:

1. Controversies regarding adult recollections should not be allowed to obscure the fact that child sexual abuse is a complex and pervasive problem in America that has historically gone unacknowledged;

2. Most people who were sexually abused as children remember all or part of what happened to them;

3. It is possible for memories of abuse that have been forgotten for a long time to be remembered;

4. It is also possible to construct convincing pseudo-memories for events that never occurred; and

5. There are gaps in our knowledge about the processes that lead to accurate and inaccurate recollections of childhood abuse.

Many critics believe that memories may be distorted and false. Psychologist Elizabeth Loftus questions the concept of repressed memories and the possibility of them being accurate. Loftus focuses on techniques that therapists use in order to help the patients recover their memory. Such techniques include age regression, guided visualization, trance writing, dream work, body work, and hypnosis.

Loftus' research indicates that repressed memory faces problems, such as memory alteration. In one case a teenage boy was able to “conjure a memory of an event that never occurred.” According to Loftus, if a stable person could be influenced to remember an event that never occurred, an emotionally stressed person would be even more susceptible.

The prognosis of "pure" TGA is very good. It does not affect mortality or morbidity and unlike earlier understanding of the condition, TGA is not a risk factor for stroke or ischemic disease. Rates of recurrence are variously reported, with one systematic calculation suggesting the rate is under 6% per year. TGA "is universally felt to be a benign condition which requires no further treatment other than reassurance to the patient and his or her family."

"The most important part of management after diagnosis is looking after the psychological needs of the patient and his or her relatives. Seeing a once competent and healthy partner, sibling or parent become incapable of remembering what was said only a minute ago is very distressing, and hence it is often the relatives who will require reassurance."

TGA may have multiple etiologies and prognoses. Atypical presentations may masquerade as epilepsy and be more properly considered TEA. In addition to such probable TEA cases, some people experiencing amnestic events diverging from the diagnostic criteria articulated above may have a less benign prognosis than those with "pure" TGA.

Recently, moreover, both imaging and neurocognitive testing studies question whether TGA is as benign as has been thought. MRI scans of the brain in one study showed that among people who had experienced TGA, all had cavities in the hippocampus, and these cavities were far more numerous, larger, and more suggestive of pathological damage than in either healthy controls or a large control group of people with tumor or stroke. Verbal and cognitive impairments have been observed days after TGA attacks, of such severity that the researchers estimated the effects would be unlikely to resolve within a short time frame. A large neurocognitive study of patients more than a year after their attack has shown persistent effects consistent with amnestic mild cognitive impairment (MCI-a) in a third of the people who had experienced TGA. In another study, "selective cognitive dysfunctions after the clinical recovery" were observed, suggesting a prefrontal impairment. These dysfunctions may not be in memory "per se" but in retrieval, in which speed of access is part of the problem among people who have had TGA and experience ongoing memory problems.