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 ; .

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.

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).

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.

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.

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.

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 most prominent symptom of post-traumatic amnesia (PTA) is a loss of memory of the present time. As a result, patients are often unaware of their condition and may behave as if they are going about their regular lives. This can cause complications if patients are confined to a hospital and may lead to agitation, distress and/or anxiety. Many patients report feeling as though they were being "held prisoner" and being prevented from carrying on with their daily lives. Other symptoms include agitation, confusion, disorientation, and restlessness.

Patients also often display behavioral disturbances. Patients may shout, swear and behave in a disinhibited fashion. There have been cases in which patients who do not recognize anyone will ask for family members or acquaintances that they have not seen in years. Some patients exhibit childlike behavior. Other patients show uncharacteristically quiet, friendly and loving behavior. Although this behavior may seem less threatening because of its lack of aggressiveness, it may be equally worrisome.

PTA patients are often unaware of their surroundings and will ask questions repeatedly. Patients may also have a tendency to wander off, which can be a major concern in those who have suffered additional injuries at the time of trauma, such as injured limbs, as it may lead to the worsening of these secondary injuries.

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.

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.

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.

Drug-induced amnesia is amnesia caused by drugs. Amnesia may be therapeutic for medical treatment or for medical procedures, or it may be a side-effect of a drug, such as alcohol, or certain medications for psychiatric disorders, such as benzodiazepines.

Post-traumatic amnesia (PTA) is a state of confusion that occurs immediately following a traumatic brain injury in which the injured person is disoriented and unable to remember events that occur after the injury. The person may be unable to state his or her name, where he or she is, and what time it is. When continuous memory returns, PTA is considered to have resolved. While PTA lasts, new events cannot be stored in the memory. About a third of patients with mild head injury are reported to have "islands of memory", in which the patient can recall only some events. During PTA, the patient's consciousness is "clouded". Because PTA involves confusion in addition to the memory loss typical of amnesia, the term "post-traumatic confusional state" has been proposed as an alternative.

There are two types of amnesia: retrograde amnesia (loss of memories that were formed shortly before the injury) and anterograde amnesia (problems with creating new memories after the injury has taken place). Both retrograde and anterograde forms may be referred to as PTA, or the term may be used to refer only to anterograde amnesia.

A common example in sports concussion is the quarterback who was able to conduct the complicated mental tasks of leading a football team after a concussion, but has no recollection the next day of the part of the game that took place after the injury. Retrograde amnesia sufferers may partially regain memory later, but memories are not regained with anterograde amnesia because they were not encoded properly.

The term "post-traumatic amnesia" was first used in 1940 in a paper by Symonds to refer to the period between the injury and the return of full, continuous memory, including any time during which the patient was unconscious.

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 person having an attack of TGA has almost no capacity to establish new memories, but generally appears otherwise mentally alert and lucid, possessing full knowledge of self-identity and identity of close family, and maintaining intact perceptual skills and a wide repertoire of complex learned behavior. The individual simply cannot recall anything that happened outside the last few minutes, while memory for more temporally distant events may or may not be largely intact. The degree of amnesia is profound, and, in the interval during which the individual is aware of his or her condition, is often accompanied by anxiety.

The diagnostic criteria for TGA, as defined for purposes of clinical research, include:

- The attack was witnessed by a capable observer and reported as being a definite loss of recent memory (anterograde amnesia).

- There was an absence of clouding of consciousness or other cognitive impairment other than amnesia.

- There were no focal neurological signs or deficits during or after the attack.

- There were no features of epilepsy, or active epilepsy in the past two years, and the patient did not have any recent head injury.

- The attack resolved within 24 hours.

This onset of TGA is generally fairly rapid, and its duration varies but generally lasts between 2 and 8 hours. A person experiencing TGA typically has memory only of the past few minutes or less, and cannot retain new information beyond that period of time. One of its bizarre features is perseveration, in which the victim of an attack faithfully and methodically repeats statements or questions, complete with profoundly identical intonation and gestures "as if a fragment of a sound track is being repeatedly rerun." This is found in almost all TGA attacks and is sometimes considered a defining characteristic of the condition. The individual experiencing TGA retains social skills and older significant memories, almost always including knowing his or her own identity and the identity of family members, and the ability to perform various complex learned tasks including driving and other learned behavior; one individual "was able to continue putting together the alternator of his car." Though outwardly appearing to be normal, a person with TGA is disoriented in time and space, perhaps knowing neither the year nor where they reside. Although confusion is sometimes reported, others consider this an imprecise observation, but an elevated emotional state (compared to patients experiencing Transient Ischemic Attack, or TIA) is common. In a large survey, 11% of individuals in a TGA state were described as exhibiting "emotionalism" and 14% "fear of dying". The attack lessens over a period of hours, with older memories returning first, and the repetitive fugue slowly lengthening so that the victim retains short-term memory for longer periods. While seemingly back to normal within 24 hours, there are subtle effects on memory that can persist longer. In the majority of cases there are no long-term effects other than a complete lack of recall for this period of the attack and an hour or two before its onset.

There is emerging evidence for observable impairments in a minority of cases weeks or even years following a TGA attack.

There is also evidence that the victim is aware that something is not quite right, even though they can't pinpoint it. Persons suffering from the attack may vocalize signs that 'they just lost their memory', or that they believed they had a stroke, although they aren't aware of the other signs that they are displaying. The main sign of this condition is the repetitive actions of something that is not usually repeated.

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.

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.

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.

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.

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.

Agnosia is the inability to recognize certain objects, persons or sounds. Agnosia is typically caused by damage to the brain (most commonly in the occipital or parietal lobes) or from a neurological disorder. Treatments vary depending on the location and cause of the damage. Recovery is possible depending on the severity of the disorder and the severity of the damage to the brain. Many more specific types of agnosia diagnoses exist, including: associative visual agnosia, astereognosis, auditory agnosia, auditory verbal agnosia, prosopagnosia, simultanagnosia, topographical disorientation, visual agnosia etc.

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.

Memory disorders are the result of damage to neuroanatomical structures that hinders the storage, retention and recollection of memories. Memory disorders can be progressive, including Alzheimer's disease, or they can be immediate including disorders resulting from head injury.