To install click the Add extension button. That's it.

The source code for the WIKI 2 extension is being checked by specialists of the Mozilla Foundation, Google, and Apple. You could also do it yourself at any point in time.

4,5
Kelly Slayton
Congratulations on this excellent venture… what a great idea!
Alexander Grigorievskiy
I use WIKI 2 every day and almost forgot how the original Wikipedia looks like.
What we do. Every page goes through several hundred of perfecting techniques; in live mode. Quite the same Wikipedia. Just better.
.
Leo
Newton
Brights
Milds

From Wikipedia, the free encyclopedia

Amnesia
SynonymsAmnesic syndrome
SpecialtyPsychiatry, Neurology

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.[citation needed]

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.[citation needed] In people suffering with amnesia, the ability to recall immediate information is still retained,[4][full citation needed][better source needed] 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'.

YouTube Encyclopedic

  • 1/1
    Views:
    52 822
  • ✪ Amnesia - causes, symptoms, diagnosis, treatment, pathology

Transcription

In the movie The Bourne Identity, CIA assassin Jason Bourne tells his new acquaintance Marie Kreutz about washing up on shore, unconscious, with two bullets in his back. He tells her that he can’t remember anything that happened before regaining consciousness, saying [Jason: No, I’m serious. I don’t know who I am, I don’t know where I’m going, none of it.] Jason Bourne has amnesia which refers to lacking memory. Now, memory can be divided into two main types. The first is implicit memory, also known as procedural memory. Procedural memory refers the sorts of skills you do automatically, without thinking much about it. For example, walking, riding a bike, or texting for most teenagers--anything that has become a habit. The second type of memory is explicit memory, also known as declarative memory. Declarative memory refers to retaining facts--the sort of stuff you need to win a trivia contest. And these memories do take conscious effort to retrieve. When trying to remember things like, “how many countries start with the letter J?”, most of us need to stop and focus. It’s three by the way. You can think of procedural memory as “remembering how,” and declarative memory as “remembering what.” When we talk about amnesia, we really mean that some part of a person’s declarative memory, the “remembering what” is affected. Jason Bourne may not remember who he is, but he has no problem remembering how to speak foreign languages or how to fight. Now, the process of making declarative memory can be broken down into four stages, and each stage involves specific parts of the brain. The first stage is encoding, and it occurs in the prefrontal cortex. Encoding begins right when you first sense something. Say you’re tasting a strawberry. Encoding would involve classifying the strawberry according to sweetness, size, color and texture. Think of encoding as a process of breaking down an experience into a manageable parts for rest of the brain to use. The second stage is consolidation. Consolidation occurs in the hippocampus, which is deep within the temporal lobes. In consolidation, the encoded bits of information like sweetness, size, and texture of the strawberry are linked up to existing memories. Think of consolidation as solidifying the memory. Comparing that information about the strawberry with memories you already have, like eating a raspberry or a blueberry, helps determine where to put that new information in your memory. When you consolidate a memory you are organizing it in a way that will be easier to recall. The third stage is storage, and it takes place throughout the cortex. In storage, the information that gets linked up to existing memories get preserved or retained. Now in order to retain a memory, it has to be edited, pared down and simplified. So less important details, like what you were wearing or what day of the week it was when you tasted the strawberry, get edited out. That way the memory stays focused on the really important stuff the sweetness, size, color and texture of the strawberry - the stuff that matters. The fourth stage is retrieval, and it occurs in the prefrontal cortex, hippocampus, and cortex. In retrieval, the brain goes through encoding, consolidation, and storage of the memory over and over again. And with each run-through, retrieval gets easier. If you’ve ever tried to memorize facts for a test, you’ve gone through the process of retrieval. and you probably know that the more you run through that information,the more likely you’ll be able to remember it on the test. The retrieval stage protects memories from being lost - the oldest, most retrieved memories are most resilient. Now, with amnesia, any of these four stages can be affected. Amnesia can be categorized into two types, according to which stages are impacted. The first type is anterograde amnesia and it refers to an inability to form new memories - often forgetting what happened hour to hour. This can feel incredibly confusing and frustrating for individuals as they struggle to recall recent events like who they just spoke to or where they just came from. Anterograde amnesia is usually because of a problem in the encoding or consolidating stage, and typically results from damage to the prefrontal cortex or hippocampus. The second and probably most well-known type of amnesia is retrograde amnesia, and it refers to an inability to recall old memories. This can cause anxiety for individuals with retrograde amnesia as well as friends and family as they completely forget important people or moments in their life. Often, individuals might create false memories, called confabulations, or might have difficulty placing a specific memory in time. Retrograde amnesia is usually because of a problem in the storage or retrieval stage, and typically results from damage to the cortex, but could involve the prefrontal cortex or hippocampus as well. Both anterograde and retrograde amnesia can be caused by acute and chronic conditions. Acute causes include traumatic head wounds or infections. And Chronic causes include brain tumors and neurodegenerative diseases, including dementia and alzheimer’s. Amnesia can also develop from a thiamine or vitamin B1 deficiency, and in that setting it’s called Wernicke-Korsakoff syndrome. Amnesia can also result from medical procedures like electroconvulsive therapy, as well as medications like benzodiazepines. Besides brain injury or illness, retrograde amnesia can result from psychological trauma, in which case it’s termed dissociative amnesia. It’s unclear how psychological trauma causes retrograde amnesia, but it’s thought that perhaps forgetting traumatic events is a psychological defense against the distress they can cause. Sometimes dissociative amnesia targets a specific memory, like a specific violent event, whereas other times it can be more general, wiping out whole decades of memories. Sometimes dissociative amnesia is accompanied by dissociative fugue, where a person suddenly wanders away from their home or community without a clear memory of having done that. Diagnosis of amnesia often requires getting a medical history from the person affected, as well as their friends and family to help fill in possible gaps. Blood tests can detect nutritional deficiencies or infections that impact memory. And MRI or a CT imaging may be used to detect structural damage or abnormalities in the brain. For a diagnosis of dissociative amnesia, the Diagnostic and Statistical Manual of Mental Disorders, or DSM-V, states that memory loss should “not occur exclusively during the course” of dissociative fugue, meaning that the memory loss should still be present after the episode of wandering away is over. The DSM-V further states that the amnesia can’t be “due to any physiologic effects” of a drug, or be better explained by any other medical condition associated with retrograde amnesia. In many cases, amnesia is temporary, and people will regain memory so long as the cause is addressed. Occupational and cognitive therapies can assist with the recovery process, by teaching people strategies for organizing and sorting new information, and help those with amnesia learn to manage day-to-day life. Mobile phones and other portable digital devices have become an important part of treatment, as they can provide people with alarms and other reminders, as well as a way to store important information, like pictures and videos of close friends and family. For dissociative amnesia, psychotherapy can help a person safely process traumatic memories. Alright, so as a quick recap, anterograde amnesia usually affects the encoding or consolidating stage of memory formation and causes a person to be unable to form new memories. Retrograde amnesia usually affects the storage or retrieval stage of memory formation and causes a person to be unable to recall old memories. One type of retrograde amnesia is a dissociative amnesia which is thought to be a psychological defense to dissociate or detach from distressing events in the past.

Contents

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][better source needed]

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][better source needed]

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][better source needed] Retrograde amnesia is usually temporary and can be treated by exposing them to memories from the loss.[16][better source needed] 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][better source needed] 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][unreliable medical source?]
  • 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][unreliable medical source?] 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][unreliable medical source?] 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][better source needed] 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.[citation needed]

See also

References

  1. ^ a b c d e Gazzaniga, M., Ivry, R., & Mangun, G. (2009) Cognitive Neuroscience: The biology of the mind. New York: W.W. Norton & Company.
  2. ^ "Amnesia." The Gale Encyclopedia of Science. Ed. K. Lee Lerner and Brenda Wilmoth Lerner. 4th ed. Vol. 1. Detroit: Gale, 2008. 182–184. Gale Virtual Reference Library.
  3. ^ Schacter, Daniel. L "Psychology"
  4. ^ D. Frank Benson, "AMNESIA"
  5. ^ LS., Cermak (1984). The episodic-semantic distinction in amnesia. New York: Guilford Press. p. 55.
  6. ^ M, Kinsbourne (1975). Short-term memory processes and the amnesic syndrome. New York: Academic. pp. 258–91.
  7. ^ H, Weingartner (1983). Forms of cognitive failure. Sc alzheimerience. pp. 221:380–2.
  8. ^ Myers, David G. Psychology. fifth ed. New York: Worth Publishers, 1998. N. pag. Print
  9. ^ Benbow, SM (2004) "Adverse effects of ECT". In AIF Scott (ed.) The ECT Handbook, second edition. London: The Royal College of Psychiatrists, pp. 170–174.
  10. ^ Goodwin DW; Crane JB; Guze SB (August 1969). "Alcoholic "blackouts": a review and clinical study of 100 alcoholics". Am J Psychiatry. 126 (2): 191–8. doi:10.1176/ajp.126.2.191. PMID 5804804.
  11. ^ Parker ES; Birnbaum IM; Noble EP (December 1976). "Alcohol and memory: Storage and state dependency". Journal of Verbal Learning and Verbal Behaviour. 15 (6): 691–702. doi:10.1016/0022-5371(76)90061-X.
  12. ^ Carlson, N. R. (19992000). Memory. Psychology: the science of behaviour (Canandian ed., p. 250). Scarborough, Ont.: Allyn and Bacon Canada.
  13. ^ a b Erdogan, Serap (2010). "Anterograde Amnesia" (PDF). Psikiyatride Guncel Yaklasimlar-Current Approaches in Psychiatry. 2 (2): 174–189. Retrieved 27 November 2011.
  14. ^ Barash, Jed A.; Ganetsky, Michael; Boyle, Katherine; Raman, Vinod; Toce, Michael S.; Kaplan, Scott; Lev, Michael H.; Worth, Jonathan L.; DeMaria, Alfred (2018). "Acute Amnestic Syndrome Associated with Fentanyl Overdose". New England Journal of Medicine. 378 (12): 1157–1158. doi:10.1056/NEJMc1716355. ISSN 1533-4406. PMID 29562161.
  15. ^ Mastin, L. (2010). The human memory: Retrograde amnesia . Retrieved from http://www.human-memory.net/disorders_retrograde.html
  16. ^ "memory abnormality." Encyclopædia Britannica. Encyclopædia Britannica Online Academic Edition. Encyclopædia Britannica Inc., 2012. Web. 21 April 2012.
  17. ^ Masferrer, Roberto; Masferrer, Mauricio; Prendergast, Virginia; Harrington, Timothy R (2000). "Grading Scale for Cerebral Concussions". BNI Quarterly. 16 (1). ISSN 0894-5799. Retrieved 5 February 2017.
  18. ^ "Dissociative Fugue. Retrieved 7 August 2012". My.clevelandclinic.org. Archived from the original on 4 November 2012. Retrieved 22 December 2012.
  19. ^ "The Merck Manuals Online". Merckmanuals.com. Retrieved 22 December 2012.
  20. ^ Carlson, Neil (2007). Psychology the Science of Behaviour. Toronto: Pearson. p. 283. ISBN 978-0-205-64524-4. OCLC 441151384.
  21. ^ Hayne, Harlene; Jack, Fiona (2011). "Childhood amnesia". Wiley Interdisciplinary Reviews: Cognitive Science. 2 (2): 136–145. doi:10.1002/wcs.107. PMID 26302005.
  22. ^ Schacter, D.L.; Harbluk, J.L.; McLachlen, D.R. (1984). "Retrieval without recollection: an experimental analysis of source amnesia". Journal of Verbal Learning and Verbal Behaviour. 23 (5): 593–611. doi:10.1016/s0022-5371(84)90373-6.
  23. ^ "Types of Amnesia". uwaterloo. Archived from the original on 20 April 2012. Retrieved 9 April 2012.
  24. ^ Walsh RD, Jr; Wharen RE, IV; Tatum WO (2011). "Complex transient epileptic amnesia". Epilepsy & Behavior. 20 (2): 410–413. doi:10.1016/j.yebeh.2010.12.026.
  25. ^ Murray, B. D.; Kensinger, E. A. (2012). "Semantic Memory in Profound Amnesia". Encyclopedia of the Sciences of Learning. Boston, MA: Springer. pp. 3022–3025.
  26. ^ a b Nordqvist, Christian (21 January 2017) [2004]. "Amnesia: Causes, Symptoms, and Treatments". Medical News Today. Retrieved 5 February 2017.
  27. ^ a b "Treating Amnesia". Neurology Now. 4 (4): 37. 2008. doi:10.1097/01.NNN.0000333846.54546.f8. Retrieved 22 December 2012.
  28. ^ a b c Mayo Clinic Staff (2011) Amnesia: Treatments and Drugs. Mayo Clinic. Retrieved from: http://www.mayoclinic.com/health/amnesia/DS01041/DSECTION=treatments-and-drugs.
  29. ^ Mandal, A. (n.d) Treatment of Amnesia. News Medical. Retrieved From: http://www.news-medical.net/health/Treatment-of-amnesia.aspx
  30. ^ Benson DF (October 1978). "Amnesia". Southern Medical Journal. 71 (10): 1221–1227. doi:10.1097/00007611-197810000-00011. ISSN 0038-4348. PMID 360401.
  31. ^ Ribot, T. (1882). Diseases of Memory: An essay in the positive psychology. London: D. Appleton and company.
  32. ^ Scoville, W.B.; Milner, B. (1957). "Loss of recent memory after bilateral hippocampal lesions". Journal of Neurology, Neurosurgery, and Psychiatry. 20 (1): 11–21. doi:10.1136/jnnp.20.1.11. PMC 497229. PMID 13406589.
  33. ^ a b Corkin, S.; Milner, B.; Teuber, H. (1968). "Further Analysis of the Hippocampal Amnesic Syndrome: 14-Year Follow-up Study on Patient H.M." (PDF). Neuropsychologia. 6 (3): 215–234. doi:10.1016/0028-3932(68)90021-3.
  34. ^ a b Draaisma, D. (2013). "Neuroscience: Losing the past". Nature. 497 (7449): 313–314. doi:10.1038/497313a.
  35. ^ Rosenbaum, R. S.; Murphy, K. J.; Rich, J. B. (2012). "The amnesias". Wiley Interdisciplinary Reviews: Cognitive Science. 3 (1): 47–63. doi:10.1002/wcs.155. PMID 26302472.
  36. ^ Zola-Morgan, S; Squire, LR; Amaral, DG (1986). "Human amnesia and the medial temporal region: Enduring memory impairment following a bilateral lesion limited to field CA1 of the hippocampus". The Journal of Neuroscience. 6 (10): 2950–2967. doi:10.1523/JNEUROSCI.06-10-02950.1986. PMID 3760943.
  37. ^ Rempel-Clower, NL; Zola, SM; Squire, LR; Amaral, DG (1996). "Three cases of enduring memory impairment after bilateral damage limited to the hippocampal formation". The Journal of Neuroscience. 16 (16): 5233–5255. doi:10.1523/JNEUROSCI.16-16-05233.1996. PMID 8756452.
  38. ^ a b Lethem, Jonathan (ed.) The Vintage Book of Amnesia New York: Vintage, 2000 ISBN 0-375-70661-5

External links

Classification
External resources
This page was last edited on 13 March 2019, at 23:39
Basis of this page is in Wikipedia. Text is available under the CC BY-SA 3.0 Unported License. Non-text media are available under their specified licenses. Wikipedia® is a registered trademark of the Wikimedia Foundation, Inc. WIKI 2 is an independent company and has no affiliation with Wikimedia Foundation.