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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

Epilepsy surgery has been performed since the 1860s and doctors have observed that it is highly effective in producing freedom from seizures. However, it was not until 2001 that a scientifically sound study was carried out to examine the effectiveness of temporal lobectomy.

Temporal lobe surgery can be complicated by decreased cognitive function. However, after temporal lobectomy, memory function is supported by the opposite temporal lobe; and recruitment of the frontal lobe. Cognitive rehabilitation may also help.

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.

The diagnosis of temporal lobe epilepsy can include the following methods: Magnetic resonance imaging (MRI), CT scans, positron emission tomography (PET), EEG, and magnetoencephalography.

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 ; .

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).

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

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

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.

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

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

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

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

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

The risk of awareness is reduced by avoidance of paralytics unless necessary; careful checking of drugs, doses and equipment; good monitoring, and careful vigilance during the case. The Isolated Forearm Technique (IFT) can be used to monitor consciousness; the technique involves applying a tourniquet to the patient's upper arm before the administration of muscle relaxants, so that the forearm can still be moved consciously. The technique is considered a reference standard by which other means of assessing consciousness can be assessed.

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.