Amnesia

Amnesia is a deficit in memory caused by brain damage, disease, or psychological trauma.[1] 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.[2] 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.[3] 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,[4] 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.[1] 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.[5][6][7]

The term is from Ancient Greek, meaning 'forgetfulness'; from ἀ- (a-), meaning 'without', and μνήσις (mnesis), meaning 'memory'.

Amnesia
SynonymsAmnesic syndrome
SpecialtyPsychiatry, Neurology

Signs and symptoms

People with amnesia can learn new information, particularly non-declarative knowledge. However, some people with dense anterograde amnesia do not remember the episodes during which they learned or observed the information previously.

Declarative information

Some patients with anterograde amnesia can still acquire some semantic information, even though it might be more difficult and might remain rather unrelated to more general knowledge. H.M. could accurately draw a floor plan of the home in which he lived after surgery, even though he had not lived there in years. The reason patients could not form new episodic memories is likely because the CA1 region of the hippocampus was a lesion, and thus the hippocampus could not make connections to the cortex. After an ischemic episode following surgery, an MRI of patient R.B. showed his hippocampus to be intact except for a specific lesion restricted to the CA1 pyramidal cells.[1]

Non-declarative information

Some retrograde and anterograde amnesics are capable of non-declarative memory, including implicit learning and procedural learning. For example, some patients show improvement on the pseudorandom sequences experiment as healthy people do. Therefore, procedural learning can proceed independently of the brain system required for declarative memory. According to fMRI studies, the acquisition of procedural memories activates the basal ganglia, the premotor cortex and the supplementary motor area, regions which are not normally associated with the formation of declarative memories. This type of dissociation between declarative and procedural memory can also be found in patients with diencephalic amnesia such as Korsakoff's syndrome. Another example demonstrated by some patients, such as K.C. and H.M, who have medial temporal damage and anterograde amnesia, still have perceptual priming. Those patients did well in the word fragment completion test.[1]

Causes

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 subcategory 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 is more often seen from events like this, an exact example of a cause of the two would be electroconvulsive 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.[8] 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.

Among specific causes of amnesia are the following:

Diagnosis

Types

  • Anterograde amnesia is the inability to create new memories due to brain damage, while long-term memories from before the event remain intact. The brain damage can be caused by the effects of long-term alcoholism, severe malnutrition, stroke, head trauma, encephalitis, surgery, Wernicke–Korsakoff syndrome, cerebrovascular events, anoxia or other trauma.[12] The two brain regions related with this condition are medial temporal lobe and medial diencephalon. Anterograde amnesia cannot be treated with pharmacological methods due to neuronal loss.[13] However, treatment exists in educating patients to define their daily routines and after several steps they begin to benefit from their procedural memory. Likewise, social and emotional support is critical to improving quality of life for anterograde amnesia sufferers.[13] Fentanyl use by opioid users has been identified as a potential cause in a cluster of cases that occurred in Boston, MA.[14]
  • Retrograde amnesia is inability to recall memories before onset of amnesia. One may be able to encode new memories after the incident. Retrograde is usually caused by head trauma or brain damage to parts of the brain besides the hippocampus. The hippocampus is responsible for encoding new memory. Episodic memory is more likely to be affected than semantic memory. The damage is usually caused by head trauma, cerebrovascular accident, stroke, tumor, hypoxia, encephalitis, or chronic alcoholism. People suffering from retrograde amnesia are more likely to remember general knowledge rather than specifics. Recent memories are less likely to be recovered, but older memories will be easier to recall due to strengthening over time.[15] Retrograde amnesia is usually temporary and can be treated by exposing them to memories from the loss.[16] Another type of consolidation (process by which memories become stable in the brain) occurs over much longer periods of time/days, weeks, months and years and likely involves transfer of information from the hippocampus to more permanent storage site in the cortex. The operation of this longer-term consolidation process is seen in the retrograde amnesia of patients with hippocampal damage who can recall memories from childhood relatively normally, but are impaired when recalling experiences that occurred just a few years prior to the time they became amnesic. (Kirwan et al.,2008)
  • Post-traumatic amnesia is generally due to a head injury (example: a fall, a knock on the head). Traumatic amnesia is often transient, but may be permanent or either anterograde, retrograde, or mixed type. The extent of the period covered by the amnesia is related to the degree of injury and may give an indication of the prognosis for recovery of other functions. Mild trauma, such as a car accident that results in no more than mild whiplash, might cause the occupant of a car to have no memory of the moments just before the accident due to a brief interruption in the short/long-term memory transfer mechanism. The sufferer may also lose knowledge of who people are. Having longer periods of amnesia or consciousness after an injury may be an indication that recovery from remaining concussion symptoms will take much longer.[17]
  • Dissociative amnesia results from a psychological cause as opposed to direct damage to the brain caused by head injury, physical trauma or disease, which is known as organic amnesia. Dissociative amnesia can include:
    • Repressed memory is the inability to recall information, usually about stressful or traumatic events in persons' lives, such as a violent attack or disaster. The memory is stored in long-term memory, but access to it is impaired because of psychological defense mechanisms. Persons retain the capacity to learn new information and there may be some later partial or complete recovery of memory. Formerly known as "Psychogenic Amnesia".
    • Dissociative fugue (formerly psychogenic fugue) is also known as fugue state. It is caused by psychological trauma and is usually temporary and unresolved, and therefore may return. An individual with dissociative fugue disorder is unaware or confused about his or her identity and will travel in journeys away from familiar surroundings to discover or create new identities.[18] The Merck Manual defines it as "one or more episodes of amnesia in which patients cannot recall some or all of their past and either lose their identity or form a new identity. The episodes, called fugues, result from trauma or stress. Dissociative fugue often manifests as sudden, unexpected, purposeful travel away from home."[19] While popular in fiction, it is extremely rare.
    • Posthypnotic amnesia occurs when events during hypnosis are forgotten, or where past memories are unable to be recalled. The failure to remember those events is induced by suggestions made during the hypnosis.[20]
  • Lacunar amnesia is the loss of memory about one specific event.
  • Childhood amnesia (also known as infantile amnesia) is the common inability to remember events from one's own childhood. Sigmund Freud notoriously attributed this to sexual repression, while modern scientific approaches generally attribute it to aspects of brain development or developmental psychology, including language development, which may be why people do not easily remember pre-language events. Researchers have found that implicit memories cannot be recalled or described. Remembering how to play the piano is a common example of implicit memory, as is walking, speaking and other everyday activities that would be difficult to focus on if they had to be relearned every time one got up in the morning. Explicit memories, on the other hand, can be recalled and described in words. Remembering the first time meeting a teacher is an example of explicit memories.[21]
  • Transient global amnesia is a well-described medical and clinical phenomenon. This form of amnesia is distinct in that abnormalities in the hippocampus can sometimes be visualized using a special form of magnetic resonance imaging of the brain known as diffusion-weighted imaging (DWI). Symptoms typically last for less than a day and there is often no clear precipitating factor or any other neurological deficits. The cause of this syndrome is not clear. The hypothesis of the syndrome includes transient reduced blood flow, possible seizure or an atypical type of a migraine. Patients are typically amnestic of events more than a few minutes in the past, though immediate recall is usually preserved.
  • Source amnesia is the inability to remember where, when or how previously learned information has been acquired, while retaining the factual knowledge.[22]
  • Korsakoff's syndrome can result from long-term alcoholism or malnutrition. It is caused by brain damage due to a vitamin B1 deficiency and will be progressive if alcohol intake and nutrition pattern are not modified. Other neurological problems are likely to be present in combination with this type of Amnesia. Korsakoff's syndrome is also known to be connected with confabulation. The person's short-term memory may appear to be normal, but the person may have a difficult time attempting to recall a past story, or with unrelated words, as well as complicated patterns.[23]
  • Drug-induced amnesia is intentionally caused by injection of an amnestic drug to help a patient forget surgery or medical procedures, particularly those not performed under full anesthesia, or likely to be particularly traumatic. Such drugs are also referred to as "premedicants". Most commonly, a 2-halogenated benzodiazepine such as midazolam or flunitrazepam is the drug of choice, although other strongly amnestic drugs such as propofol or scopolamine may also be used for this application. Memories of the short time-frame in which the procedure was performed are permanently lost or at least substantially reduced, but once the drug wears off, memory is no longer affected.
  • Situation-specific amnesia can arise in a variety of circumstances (for example, committing an offence, child sexual abuse) resulting in PTSD. It has been claimed that it involves a narrowing of consciousness with attention focused on central perceptual details and/or that the emotional or traumatic events are processed differently from ordinary memories.
  • Transient epileptic amnesia is a rare and unrecognized form of temporal lobe epilepsy, which is typically an episodic isolated memory loss. It has been recognized as a treatment-responsive syndrome congenial to anti-epileptic drugs.[24]
  • Semantic amnesia affects semantic memory and primarily expresses itself in the form of problems with language use and acquisition.[25]

Treatment

Many forms of amnesia fix themselves without being treated.[26] 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.[27] This may also include strategies for organizing information to remember it more easily and for improving understanding of lengthy conversation.[28]

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.[27] Notebooks, wall calendars, pill reminders and photographs of people and places are low-tech memory aids that can help as well.[28]

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.[29] 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.[26] Treating alcoholism and preventing alcohol and illicit drug use can prevent further damage, but in most cases will not recover lost memory.[28]

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.[30]

History

French psychologist Theodule-Armand Ribot was among the first scientists to study amnesia. He proposed Ribot's Law which states that there is a time gradient in retrograde amnesia. The law follows a logical progression of memory loss due to disease. First, a patient loses the recent memories, then personal memories, and finally intellectual memories. He implied that the most recent memories were lost first.[31]

Case studies have played a large role in the discovery of amnesia and the parts of the brain that were affected. The studies gave important insight into how amnesia affects the brain. The studies also gave scientists the resources into improving their knowledge about amnesia and insight into a cure or prevention. There are several extremely important case studies: Henry Molaison, R.B, and G.D.

Henry Molaison

Henry Molaison, formerly known as H.M., changed the way people thought of memory. The case was first reported in a paper by William Beecher Scoville and Brenda Milner in 1957.[32] He was a patient who suffered from severe epilepsy attributed to a bicycle accident at the age of nine. Physicians were unable to control his seizures with drugs, so the neurosurgeon Scoville tried a new approach involving brain surgery. He removed his medial temporal lobe bilaterally by doing a temporal lobectomy. His epilepsy did improve, but Molaison lost the ability to form new long-term memories (anterograde amnesia). He exhibited normal short-term memory ability. If he was given a list of words, he would forget them in about a minute's time. In fact, he would forget that he was even given a list in the first place.[33] Once Molaison stopped thinking about the lists he was unable to recall them again from long term memory. This gave researchers evidence that short-term and long-term memory are in fact two different processes.[34] Even though he forgot about the lists, he was still able to learn things through his implicit memory. The psychologists would ask him to draw something on a piece of paper, but to look at the paper using a mirror. Though he could never remember ever doing that task, he would improve after doing it over and over again. This showed the psychologists that he was learning and remembering things unconsciously.[35]

Studies were completed consistently throughout Molaison's lifetime to discover more about amnesia.[1] Researchers did a 14-year follow-up study on Molaison. They studied him for a period of two weeks to learn more about his amnesia. After 14 years, Molaison still could not recall things that had happened since his surgery. However, he could still remember things that had happened prior to the operation. Researchers also found that, when asked, Molaison could answer questions about national or international events, but he could not remember his own personal memories.[33] After his death Molaison donated his brain to science, where they were able to discover the areas of the brain that had the lesions which caused his amnesia.[34] This case study provided important insight to the areas of the brain that are affected in anterograde amnesia, as well as how amnesia works.

Patient R.B.

Patient R.B. was a normally functioning man until the age of 52. At age 50, he had been diagnosed with angina and had surgery for heart problems on two occasions. After an ischemic episode (reduction of blood to the brain) that was caused from a heart bypass surgery, R.B. demonstrated a loss of anterograde memory, but almost no loss of retrograde memory, with the exception of a couple of years before his surgery, and presented no sign of any other cognitive impairment. It wasn't until after his death that researchers had the chance to examine his brain, when they found his lesions were restricted to the CA1 portion of the hippocampus. This case study led to important research involving the role of the hippocampus and the function of memory.[36]

Patient G.D.

Patient G.D. was a white male born in 1940 who served in the Navy. He was diagnosed with chronic renal failure and received hemodialysis treatment for the rest of his life. In 1983, he went to the hospital for elective parathyroidectomy. He also had a left thyroid lobectomy because of the severe loss of blood in his left lobe. He began having cardiac problems as a result of the surgery and became very agitated. Even five days after being released from the hospital he was unable to remember what had happened to him. Aside from memory impairment, none of his other cognitive processes seemed to be affected. He did not want to be involved in much research, but through memory tests he took with doctors, they were able to ascertain that his memory problems were present for the next 9.5 years until his death. After he died, his brain was donated to science, photographed, and preserved for future study.[37]

In fiction

Global amnesia is a common motif in fiction despite being extraordinarily rare in reality. In the introduction to his anthology The Vintage Book of Amnesia, Jonathan Lethem writes:

Real, diagnosable amnesia – people getting knocked on the head and forgetting their names – is mostly just a rumor in the world. It's a rare condition, and usually a brief one. In books and movie, though, versions of amnesia lurk everywhere, from episodes of Mission Impossible to metafictional and absurdist masterpieces, with dozens of stops in between. Amnesiacs might not much exist, but amnesiac characters stumble everywhere through comic books, movies, and our dreams. We've all met them and been them.[38]

Lethem traces the roots of literary amnesia to Franz Kafka and Samuel Beckett, among others, fueled in large part by the seeping into popular culture of the work of Sigmund Freud, which also strongly influenced genre films such as film noir. Amnesia is so often used as a plot device in films, that a widely recognized stereotypical dialogue has even developed around it, with the victim melodramatically asking "Where am I? Who am I? What am I?", or sometimes inquiring of his own name, "Bill? Who's Bill?"[38]

In movies and television, particularly sitcoms and soap operas, it is often depicted that a second blow to the head, similar to the first one which caused the amnesia, will then cure it. In reality, however, repeat concussions may cause cumulative deficits including cognitive problems, and in extremely rare cases may even cause deadly swelling of the brain associated with second-impact syndrome.

See also

Amnesiacs

References

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External links

External resources
50 First Dates

50 First Dates is a 2004 American romantic comedy film directed by Peter Segal and written by George Wing. The film stars Adam Sandler as a veterinarian and Drew Barrymore as an amnesiac, along with Rob Schneider, Sean Astin, Lusia Strus, Blake Clark, and Dan Aykroyd. Most of the film was shot on location in Oahu, Hawaii on the Windward side and the North Shore. Sandler and Barrymore won an MTV award for Best On-Screen Team. The fictitious memory impairment suffered by Barrymore's character, Goldfield's Syndrome, is similar to short-term memory loss and anterograde amnesia. The 2014 Malayalam film Ormayundo Ee Mukham is inspired by 50 First Dates, as are the 2007 Telugu film, Sathyabhama, and the 2018 Japanese film "50 First Kisses" (50回目のファーストキス).

A Wind Named Amnesia

A Wind Named Amnesia (Japanese: 風の名はアムネジア, Hepburn: Kaze no Na wa Amunejia), also known as The Wind of Amnesia in Australia and the United Kingdom, is a Japanese novel authored by Hideyuki Kikuchi, originally published in 1983 by Asahi Sonorama. An anime film adaptation was released theatrically on December 22, 1990, directed by Kazuo Yamazaki. An English adaptation of the film was produced and released by Manga Entertainment on home video in Australia and the UK and by Central Park Media in North America.

Anterograde amnesia

Anterograde amnesia is a loss of the ability to create new memories after the event that caused 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.

Blackout (drug-related amnesia)

A drug-related blackout is a phenomenon caused by the intake of any substance or medication in which short-term and long-term memory creation is impaired, therefore causing a complete inability to recall the past. Blackouts are most frequently associated with GABAergic drugs. Blackouts are frequently described as having effects similar to that of anterograde amnesia, in which the subject cannot recall any events after the event that caused amnesia.

Research on alcohol blackouts was done by E. M. Jellinek in the 1940s. Using data from a survey of Alcoholics Anonymous (AA) members, he came to believe that blackouts would be a good determinant of alcoholism. However, there are conflicting views whether this is true. The negative psychological effects of an alcohol-related blackout are often worsened by those who suffer from anxiety disorders. Impairment of the liver will also allow more alcohol to reach the brain and hasten the individual's blackout.

The term "blackout" can also refer to a complete loss of consciousness, or syncope.

Childhood amnesia

Childhood amnesia, also called infantile amnesia, is the inability of adults to retrieve episodic memories (memories of situations or events) before the age of two to four years, as well as the period before the age of ten 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 one, 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 three or four, but it can range from two to eight years.Changes in encoding, storage and retrieval of memories during early childhood are all important when considering childhood amnesia. However, 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.

Dissociation (psychology)

Dissociation is any of a wide array of experiences from mild detachment from immediate surroundings to more severe detachment from physical and emotional experiences. The major characteristic of all dissociative phenomena involves a detachment from reality, rather than a loss of reality as in psychosis.Dissociation is commonly displayed on a continuum. In mild cases, dissociation can be regarded as a coping mechanism or defense mechanisms in seeking to master, minimize or tolerate stress – including boredom or conflict. At the nonpathological end of the continuum, dissociation describes common events such as daydreaming. Further along the continuum are non-pathological altered states of consciousness.More pathological dissociation involves dissociative disorders, including dissociative fugue and depersonalization disorder with or without alterations in personal identity or sense of self. These alterations can include: a sense that self or the world is unreal (depersonalization and derealization); a loss of memory (amnesia); forgetting identity or assuming a new self (fugue); and separate streams of consciousness, identity and self (dissociative identity disorder, formerly termed multiple personality disorder) and complex post-traumatic stress disorder.Dissociative disorders are sometimes triggered by trauma, but may be preceded only by stress, psychoactive substances, or no identifiable trigger at all. The ICD-10 classifies conversion disorder as a dissociative disorder. The Diagnostic and Statistical Manual of Mental Disorders groups all dissociative disorders into a single category.Although some dissociative disruptions involve amnesia, other dissociative events do not. Dissociative disorders are typically experienced as startling, autonomous intrusions into the person's usual ways of responding or functioning. Due to their unexpected and largely inexplicable nature, they tend to be quite unsettling.

Dissociative disorder

Dissociative disorders (DD) are conditions that involve disruptions or breakdowns of memory, awareness, identity, or perception. People with dissociative disorders use dissociation as a defense mechanism, pathologically and involuntarily. Some dissociative disorders are triggered by psychological trauma, but dissociative disorders such as depersonalization/derealization disorder may be preceded only by stress, psychoactive substances, or no identifiable trigger at all.The dissociative disorders listed in the American Psychiatric Association's DSM-5 are as follows:

Dissociative identity disorder (formerly multiple personality disorder): the alternation of two or more distinct personality states with impaired recall among personality states. In extreme cases, the host personality is unaware of the other, alternating personalities; however, the alternate personalities can be aware of all the existing personalities. This category now includes the old derealization disorder category.

Dissociative amnesia (formerly psychogenic amnesia): the temporary loss of recall memory, specifically episodic memory, due to a traumatic or stressful event. It is considered the most common dissociative disorder amongst those documented. This disorder can occur abruptly or gradually and may last minutes to years depending on the severity of the trauma and the patient.

Dissociative fugue (formerly psychogenic fugue) is now subsumed under the dissociative amnesia category. It is described as reversible amnesia for personal identity, usually involving unplanned travel or wandering, sometimes accompanied by the establishment of a new identity. This state is typically associated with stressful life circumstances and can be short or lengthy.

Depersonalization disorder: periods of detachment from self or surrounding which may be experienced as "unreal" (lacking in control of or "outside" self) while retaining awareness that this is only a feeling and not a reality.

Dissociative seizures also known as psychogenic non-epileptic seizures: seizures that are often mistaken for epilepsy but are not caused by electrical pulses in the brain and are in fact another form of dissociation. https://www.epilepsyqueensland.com.au/psychogenic-non-epileptic-seizures

The old category of dissociative disorder not otherwise specified is now split into two: Other specified dissociative disorder, and unspecified dissociative disorder. These categories are used for forms of pathological dissociation that do not fully meet the criteria of the other specified dissociative disorders, or if the correct category has not been determined.Both dissociative amnesia and dissociative fugue usually emerge in adulthood and rarely occur after the age of 50. The ICD-10 classifies conversion disorder as a dissociative disorder while the DSM-IV classifies it as a somatoform disorder.

Drug-induced amnesia

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.

Dusk Maiden of Amnesia

Dusk Maiden of Amnesia (黄昏乙女×アムネジア, Tasogare Otome × Amunejia) is a Japanese manga series, written and illustrated by the duo Maybe. It was published by Square Enix and serialized in the Monthly Gangan Joker magazine. An anime adaptation by Silver Link aired between April and June 2012. It has been licensed by Sentai Filmworks in North America.

Fugue state

Dissociative fugue, formerly fugue state or psychogenic fugue, is a dissociative disorder and a rare psychiatric disorder characterized by reversible amnesia for personal identity, including the memories, personality, and other identifying characteristics of individuality. The state can last days, months or longer. Dissociative fugue usually involves unplanned travel or wandering, and is sometimes accompanied by the establishment of a new identity. It is a facet of dissociative amnesia, according to the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5).

After recovery from a fugue state, previous memories usually return intact, and further treatment is unnecessary. Additionally, an episode of fugue is not characterized as attributable to a psychiatric disorder if it can be related to the ingestion of psychotropic substances, to physical trauma, to a general medical condition, or to dissociative identity disorder, delirium, or dementia. Fugues are precipitated by a series of long-term traumatic episodes. It is most commonly associated with childhood victims of sexual abuse who learn over time to dissociate memory of the abuse (dissociative amnesia).

Montebello Rockfest

Montebello Rockfest, formerly known as Amnesia Rockfest, is an annual outdoor Rock festival that takes place each June in Montebello, Quebec, Canada. Founded in 2005 by then 17-year-old local resident Alex Martel, it has become the largest rock music festival in Canada and one of the largest in North America.With a local population of 978 residents, the small town of Montebello attracts over 200,000 festival-goers during Rockfest. The event proposes a diverse lineup with mainstream acts, as well as cult bands, reunions, rarities and emerging talent. Aside from its lineup, Montebello Rockfest is popular for its countryside setting, camping areas, carnival vibe and nonstop parties in the village throughout the weekend.

Post-traumatic amnesia

Post-traumatic amnesia (PTA) is a state of confusion that occurs immediately following a traumatic brain injury (TBI) in which the injured person is disoriented and unable to remember events that occur after the injury. The person may be unable to state their name, where they are, 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.

Psychogenic amnesia

Psychogenic amnesia or 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.

Repressed memory

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 subconsciously, 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 for want of written proof of their existence before the nineteenth century, but its results were disputed by some psychologists, and a work discussing a repressed memory from 1786 was eventually acknowledged, though the others stand by their hypothesis.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.

Retrograde amnesia

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 temporalley grade or more permanently 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.

Selective amnesia

Selective amnesia is a type of amnesia in which the victim loses certain parts of their memory. Common elements that may be forgotten: relationships, special talents (e.g.: juggling, whistling, instrumental talents, etc.), where they live, abilities in certain areas (e.g.: a new gymnast forgetting she cannot cartwheel yet), and events such as concerts, shows, or traumatic events (e.g.: a death/suicide of a loved one or attempt on one's own life).

Transient global amnesia

Transient global amnesia (TGA) is a neurological disorder whose key defining characteristic is a temporary but almost total disruption of short-term memory with a range of problems accessing older memories. A person in a state of TGA exhibits no other signs of impaired cognitive functioning but recalls only the last few moments of consciousness, as well as possibly a few deeply encoded facts of the individual's past, such as their childhood, family, or home perhaps.Both TGA and anterograde amnesia deal with disruptions of short-term memory. However, a TGA episode generally lasts no more than 2 to 8 hours before the patient returns to normal with the ability to form new memories. A patient with anterograde amnesia may not be able to form new memories indefinitely.

Wernicke–Korsakoff syndrome

Wernicke–Korsakoff syndrome (WKS) is the combined presence of Wernicke encephalopathy (WE) and alcoholic Korsakoff syndrome. Due to the close relationship between these two disorders, people with either are usually diagnosed with WKS as a single syndrome.

The cause of the disorder is thiamine (vitamin B1) deficiency, which can cause a range of disorders including beriberi, Wernicke encephalopathy, and alcoholic Korsakoff syndrome. These disorders may manifest together or separately. WKS is usually secondary to alcohol abuse. It mainly causes vision changes, ataxia and impaired memory.Wernicke encephalopathy and WKS are most commonly seen in people who are alcoholic, and only 20% of cases are identified before death. This failure in diagnosis of WE and thus treatment of the disease leads to death in approximately 20% of cases, while 75% are left with permanent brain damage associated with WKS. Of those affected, 25% require long-term institutionalization in order to receive effective care.

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