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

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

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

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

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

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

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

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

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

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.

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.

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

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

Early research pointed to vasopressin as a potential treatment for improving the memory of patients living with post-traumatic amnesia (PTA). Lysine vasopressin, a modified form of the vasopressin molecule, had positive effects on memory when administered by injection to patients with amnesia resulting from traumatic brain injury and Korsakoff's syndrome. Subsequent animal studies with rats found similar results, particularly in aversion and avoidance learning tasks. Rats lacking adequate vasopressin, either due to genetic defect or hypophysectomy (surgical removal of the pituitary gland), exhibited significant improvements in memory and learning functions when exogenous vasopressin was administered. Particularly encouraging was the finding that a short treatment period produced long-lasting improvements, in both humans and rats. However, the animal models of PTA are highly limited, as the dimension of self-awareness and orientation is almost impossible to model adequately. PTA in animals, especially rats, is often observed post-trauma (commonly post-surgery), but it is often only measured in terms of impaired learning or unusual behavior.

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.

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

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

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

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

As mentioned earlier, anti-anxiety, antidepressants and tranquilizers are treatment medications that do not cure, but help control the symptoms of dissociative disorders. The accepted mode of treatment are atypical neuroleptics such as Abilify, Zyprexa, Seroquel and Geodon. Newer-generation anticonvulsants are also highly effective. Quetiapine is initiated at 25–50 mg PO bid and increased by 50 mg PO bid q3d until symptom resolution is achieved. The higher dose should be administered nightly due to the strong sedation effects of the medicine. Other medications such as SSRIs and SNRIs may reduce the anxiety and apprehension of the dissociation.

Keppra may be effective in treating dissociation. Doses are usually kept much lower than for the treatment of seizure disorders. Lamotrigine started at 25 mg and increased by 25 mg every 2 weeks is another option. The effects of these novel anticonvulsants is thought to be secondary to GABA modulation.

Risk factors: People who experience chronic physical, sexual or emotional childhood abuse are at a greater risk of developing dissociative disorders. Children and adults experiencing other traumatic events (including war, natural disasters, kidnapping, torture and invasive medical procedures) also may develop these conditions.

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.

The onset of Wernicke's encephalopathy is considered a medical emergency, and thus thiamine administration should be initiated immediately when the disease is suspected. Prompt administration of thiamine to patients with Wernicke's encephalopathy can prevent the disorder from developing into Wernicke–Korsakoff syndrome, or reduce its severity. Treatment can also reduce the progression of the deficits caused by WKS, but will not completely reverse existing deficits. WKS will continue to be present, at least partially, in 80% of patients. Patients suffering from WE should be given a minimum dose of 500 mg of thiamine hydrochloride, delivered by infusion over a 30-minute period for two to three days. If no response is seen then treatment should be discontinued but for those patients that do respond, treatment should be continued with a 250 mg dose delivered intravenously or intramuscularly for three to five days unless the patient stops improving. Such prompt administration of thiamine may be a life-saving measure. Banana bags, a bag of intravenous fluids containing vitamins and minerals, is one means of treatment.

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.

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

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

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

Before delirium treatment, the cause must be established. Medication such as antipsychotics or benzodiazepines can help reduce the symptoms for some cases. For alcohol or malnourished cases, vitamin B supplements are recommended and for extreme cases, life-support can be used.

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 ; .

An open study of cognitive behavior therapy has aimed to help patients reinterpret their symptoms in a nonthreatening way, leading to an improvement on several standardized measures. A standardized treatment for DPD based on cognitive behavioral principles was published in The Netherlands in 2011.

Primary depersonalization disorder is mostly refractory to current treatments. The disorder lacks effective treatment in part because it has been neglected within the field of psychiatry, which, in turn, is partly because funding has mainly been allocated to the search for cures of other illnesses, like alcoholism. However, recognizing and diagnosing the condition may in itself have therapeutic benefits, considering many patients express their problems as baffling and unique to them, but are in fact: one, recognized and described by psychiatry; and two, those affected by it are not the only individuals to be affected from the condition. A variety of psychotherapeutic techniques have been used to treat depersonalization disorder, such as cognitive behavioral therapy. Clinical pharmacotherapy research continues to explore a number of possible options, including selective serotonin reuptake inhibitors, tricyclic antidepressants, anticonvulsants, and opioid antagonists.

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.

Recovered memory therapy is a range of psychotherapy methods based on recalling memories of abuse that had previously been forgotten by the patient. The term "recovered memory therapy" is not listed in DSM-IV or used by mainstream formal psychotherapy modality. Opponents of the therapy advance the explanation that therapy can create false memories through suggestion techniques; this has not been corroborated, though some research has shown supportive evidence. Nevertheless, the evidence is questioned by some researchers. It is possible for patients who retract their claims—after deciding their recovered memories are false—to suffer post-traumatic stress disorder due to the trauma of illusory memories.

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.

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.