amnesia: Definition from Answers.com "; ANSW.AnswerTipEnabled = true; var staticFileHost="http://site.answcdn.com/main85756";var webtipfile="http://site.answcdn.com/main85756/js/web_answertip.js?ANSW.afid=10"; var loaded={}; function loadscript(filename){ if (typeof loaded[filename]=="undefined"){ loaded[filename]=true; var head = document.getElementsByTagName("head")[0]; var script; script = document.createElement('script'); script.type = 'text/javascript'; script.src = filename; head.appendChild(script); } } // Load the answer tip on the first dbClick event. jQuery(document).dblclick(dblClickHandler); function dblClickHandler(evt){ SaveDblClick(evt); loadscript(webtipfile); jQuery(document).unbind('dblclick',dblClickHandler); } // save info on click preceding the double click jQuery(document).click(clickHandler); function clickHandler(evt){ if (typeof ANSW=="undefined") { ANSW = new Object();} if (typeof ANSW.dblclick=="undefined") { ANSW.dblclick = {};} var oe = evt.originalEvent; ANSW.dblclick.rangeParent=oe.rangeParent; ANSW.dblclick.rangeOffset=oe.rangeOffset; } function SaveDblClick(evt){ if (typeof ANSW=="undefined") { ANSW = new Object();} var oe = evt.originalEvent; if (typeof ANSW.dblclick=="undefined") { ANSW.dblclick = {};} ANSW.dblclick.target=oe.target; ANSW.dblclick.srcElement=oe.srcElement; ANSW.dblclick.clientX=oe.clientX; ANSW.dblclick.clientY=oe.clientY; ANSW.dblclick.pageX=oe.pageX; ANSW.dblclick.pageY=oe.pageY; jQuery(document).unbind('click',clickHandler); }
"; var sor2 = "src='" + sor + "'"; ifr = ifr.replace("__SRC__",sor2); document.writeln(ifr);
On this page
Library
Animal Life
Business & Finance
Cars & Vehicles
Entertainment & Arts
Food & Cooking
Health
History, Politics, Society
Home & Garden
Law & Legal Issues
Literature & Language
Miscellaneous
Religion & Spirituality
Science
Sports
Technology
Travel & Places
Q & A
amnesia
American Heritage Dictionary:
amnesia
Home > Library > Literature & Language > Dictionary
(?m-n'zh?)
n.
Partial or total loss of memory, usually resulting from shock, psychological disturbance, brain injury, or illness.
[Greek amnsi, forgetfulness, probably from amnsti, from amnstos, not remembered : a-, not; see a-1 + mimnskein, mn-, to remember.]amnesiac amne'siac' (-n'z-?k', -zh-?k') or amne'sic (-z?k, -s?k) n. & adj.
amnestic amnes'tic (-n?s't?k) adj.
English
English Deutsch Espa?ol Fran?ais Italiano Tagalog
Search unanswered questions...
Browse: Unanswered questions | Most-recent questions | Reference library
Enter a question here...
Search: All sources Community Q&A Reference topics
Browse: Unanswered questions | New questions | New answers | Reference library
Featured Videos:
Top
View more Health videos
Britannica Concise Encyclopedia:
amnesia Top
Home > Library > Miscellaneous > Britannica Concise Encyclopedia
Loss of memory as a result of brain injury or deterioration, shock, fatigue, senility, drug use, alcoholism, anesthesia, illness, or neurotic reaction. Amnesia may be anterograde (in which events following the causative trauma or disease are forgotten) or retrograde (in which events preceding the trauma or disease are forgotten). It can often be traced to a severe emotional shock, in which case personal memories (in effect, identity) rather than such abilities as language skills are affected. Such amnesia seems to represent an escape from disturbing memories and is thus an example of repression; these memories can generally be recovered through psychotherapy or after the amnesic state has ended. Amnesia may occasionally last for weeks, months, or even years, a condition known as fugue.
For more information on amnesia, visit Britannica.com.
McGraw-Hill Science & Technology Encyclopedia:
Amnesia Top
Home > Library > Science > Sci-Tech Encyclopedia
A significant but relatively selective inability to remember. Amnesia can be characterized along two dimensions with respect to its onset: an inability to remember events that occurred after the onset of amnesia is referred to as anterograde amnesia, and a deficit in remembering events that occurred prior to the onset of amnesia is referred to as retrograde amnesia. Amnesia can be due to a variety of causes and can be classified according to whether the cause is primarily neurological or psychological in origin. Neurological amnesias are the result of brain dysfunction and can be transient or permanent. They are usually characterized by a severe anterograde amnesia and a relatively less severe retrograde amnesia. Transient amnesias are temporary memory disturbances and can range in duration from hours to months, depending on the cause and severity. They can be caused by epilepsy, head injury, and electroconvulsive therapy (most frequently used for the treatment of depression). In cases of transient global amnesia, an extensive amnesia that is usually sudden in onset and resolves within a day, the cause is still not known, although many believe that it is vascular in origin.
Permanent amnesia usually occurs following brain damage to either the diencephalons or the medial temporal lobe. Amnesia resulting from impairment to the medial temporal lobe can occur following anoxia, cerebrovascular accidents, head injury, and viral infections to the brain. The primary structures involved in the processing of memory within the medial temporal lobe are the hippocampus and the amygdala. One of the most common causes of diencephalic amnesia is Wernicke-Korsakoff syndrome, a disorder caused by a thiamine deficiency, usually related to chronic alcoholism.
Memory impairment that is not associated with brain damage is referred to as functional amnesia. Functional amnesia can be classified according to whether the amnesia is nonpathological or pathological. Nonpathological functional amnesia is a normal memory loss for events occurring during infancy and early childhood, sleep, hypnosis, and anesthesia. Pathological functional amnesia is an abnormal memory loss found in cases of functional retrograde amnesia and multiple personality. In contrast to neurological amnesia, pathological functional amnesia is usually associated with more severe retrograde than anterograde amnesia. See also Brain; Memory.
Oxford Companion to the Body:
amnesia Top
Home > Library > Health > World of the Body
We forget almost everything that we have, at some time, briefly remembered. Think of all the telephone numbers you have kept in mind between looking in the directory and dialling the number; of all the people and places you once knew for a few minutes but have now mostly forgotten; of every meal that you have eaten, which you could have described in detail the same day, but could not possibly remember now. Given the overwhelming flood of information that pours into our brains each day, forgetting most things is just as important as remembering some.
On the other hand, forgetfulness can become an illness, an incapacitating inability to remember things, which is called amnesia. Amnesia occurs in many situations  after head injuries, in Alzheimer's disease, and, to some extent, in all old people. But it has mainly been studied in particular patients with profound impairments of memory, despite otherwise normal cognitive ability and intelligence. These patients are said to have the amnesic syndrome, whose characteristics include: (i) severe anterograde amnesia: poor retention of new information, exhibited by difficulty in spontaneously recalling words and objects, in recognizing faces (unless they are very familiar), and in learning associations between words or things; (ii) retrograde amnesia: poor recollection of previously established memories (such as knowledge of one's childhood, and even such things as one's own name). In general, the retrograde component of clinical amnesia is less severe than the anterograde, and may be limited to a period of months or years prior to the onset of the amnesia. In some way, ancient memories are more robust than newer ones, and can persist even when new, conscious long-term memories cannot be formed.
Despite these defects in long-term memory, patients with clinical amnesia have relatively normal short-term memory span (as measured by the ability immediately to recall a list of digits). Indeed, amnesic patients are able to engage in normal conversation and recall current information so long as it is continually rehearsed. But after just a few seconds of distraction, they may forget not only what has been said but even whether they have met the person they were talking to moments before.
Not all forms of long-term learning are impaired. Motor skills (such as typing on a keyboard or driving a car) learnt prior to the onset of the illness are unaffected, and patients show residual abilities to learn new motor skills (even though they are not consciously aware of having done the motor task before). Other simple forms of memory also persist, including classical conditioning (the kind of simple learning shown by Pavlov's dogs when they salivated to the sound of a bell after it had been rung a few times before the presentation of food). The common denominator between the forms of learning still exhibited by amnesic patients is that they can all be mediated without the need for recollection of past experience: they involve what has been called procedural learning (the learning of skills) or implicit learning (unconscious learning).
The vast majority of amnesic patients are chronic alcoholics, suffering from Korsakoff's syndrome. This is due to diffuse brain damage, predominately to lower parts of the cerebral hemispheres (principally the mamillary bodies and dorso-medial nucleus of the thalamus), although there is also frequently degeneration of the frontal lobes of the cerebral cortex. The gradual deterioration of mental function is probably due to the toxic effects of alcohol, combined with thiamine deficiency. In addition to profound memory impairments, Korsakoff patients also exhibit a range of impairments shared by patients with damage to the frontal lobes, such as lack of insight into their own deficits, confabulation (inventing explanations for their difficulties), and impairments on tests of card sorting. Due to the multiple sites of damage and the diffuse nature of the brain damage it is hard to draw firm conclusions from Korsakoff patients about which particular structures in the brain contribute to memory.
Discrete damage to the brain, especially to parts of the interior surface of the temporal lobes of the cerebral hemispheres, can also cause profound anterograde amnesia. The classical example of this devastating condition is the patient known by his initials, H. M., who underwent surgery to remove the inner parts of the temporal lobe on both sides, to relieve intractable epilepsy, and has subsequently suffered deep amnesia for decades. This part of the brain includes specialized regions of cerebral cortex called the hippocampus and the amygdala, which are thought to be involved in the laying down of memories. Unfortunately this vital part of the brain seems to be particularly vulnerable: it is relatively easily damaged by hypoxia (for instance during surgical operations in which blood supply to the brain is compromised), by the degenerative changes that occur in Alzheimer's disease, and by infection in herpes simplex encephalitis. All of these conditions can produce pronounced amnesia.
Although intensively studied and extensively documented in a small group of select patients, the classical amnesic syndrome may not be completely typical of most people with amnesia. The extent of retrograde amnesia for personal recollections of the past is particularly hard to assess in the absence of any independent verification. The amount of retrograde amnesia in H. M., for example, may have been grossly underestimated. It has even been argued that there may not be a single amnesic syndrome, since patients with temporal lobe damage tend to forget information rapidly, whereas Korsakoff patients, given enough training, are able to retain information over longer periods of time.
Because of the complexity of clinical syndromes, most of our present understanding of which neural systems contribute to normal learning and memory have come from the study of animals, especially of animal models of human amnesia. It was initially believed that combined damage to the hippocampus and amygdala was necessary to produce severe anterograde amnesia, and the hippocampus in particular became the supposed seat of episodic (personal, conscious) memory. However, this view has been challenged by the discovery that damage to a neighbouring region, the rhinal cortex, which underlies the hippocampus and amygdala, was necessary and sufficient to produce memory impairments.
Behavioural studies on monkeys, analysing the effect of circumscribed damage to specific regions in the inner part of the temporal lobe, have identified several dissociable, interacting memory structures. Much research effort is presently focused on ascertaining the role of these different components. For example, current research has called into question the traditionally accepted role of the hippocampus in episodic memory and suggests instead that this structure may play a more restricted role in the memory of places, which then contributes to a broader neural memory system. Other components of this system include the amygdala, now believed to be involved in remembering whether particular stimuli are associated with rewarding or punishing events. Another important nearby structure is the perirhinal cortex, which appears to be specialized for processing knowledge about objects. The nerve fibres of the white matter within the temporal lobe, known as the temporal stem, have also been implicated in memory. However the temporal lobe is by no means the only structure involved in human learning and memory. Communication between the temporal lobe and the frontal lobe is also important and this interaction occurs via multiple routes. In fact, neither the hippocampus, amygdala, perirhinal cortex, temporal stem, nor any other single structure in the temporal lobe when damaged on its own results in dense amnesia. But this does occur when the majority of the routes by which the temporal lobe can interact with the frontal lobe are interrupted.
Detailed structural imaging of the brain of H. M., through magnetic resonance imaging (MRI), has recently confirmed the extent of bilateral damage sustained by each of the temporal lobe structures in H. M., and this has been interpreted in terms of the understanding gained from the study of animals. The damage in H. M. is entirely consistent with the predictions from animal studies  one indication of the usefulness of these models in understanding the neural systems underlying normal human learning and memory.
 Mark Buckley
Bibliography
Bolhuis, J. J. (2000). Brain, perception, memory: advances in cognitive neuroscience. Oxford University Press, Oxford.
Eysenck, M. W. (1995). Cognitive psychology: a student's handbook, (3rd edn). Erlbaum, Hove
See also brain; cerebral cortex; hypothalamus; limbic system; memory.
Oxford Dictionary of Sports Science & Medicine:
amnesia Top
Home > Library > Health > Sports Science and Medicine
Loss of memory. Amnesia can occur after a blow to the head during a contact or collision sport. The duration of post-traumatic amnesia (the duration of memory loss from the moment of injury to the onset of continuous memory) is used as a clinical measure of the extent of diffuse brain damage. A duration of up to about 10 min is quite common. Longer than this probably indicates structural damage. However, it should be recognized that any alteration of consciousness, however transient, is serious and requires a thorough medical investigation.
Columbia Encyclopedia:
amnesia Top
Home > Library > Miscellaneous > Columbia Encyclopedia
amnesia (?mn'zh?), [Gr.,=forgetfulness], condition characterized by loss of memory for long or short intervals of time. It may be caused by injury, shock, senility, severe illness, or mental disease. Some cases of amnesia involve the unconscious suppression of a painful experience and everything remindful of it including the individual's identity (see defense mechanism). Retrograde amnesia is loss of memory of events just preceding temporary loss of consciousness, as from head injury; it is evidence that memory proceeds in two stages, short term and long term. One form of the condition known as tropic amnesia, or coast memory, affecting white men in the tropics, is probably a variety of hysteria. Aphasia of the amnesic variety is caused by an organic brain condition and is not to be confused with other forms of amnesia. To cure amnesia, attempts are made to establish associations with the past by suggestion, and hypnotism is sometimes employed.
Gale Dictionary of Psychoanalysis:
Amnesia Top
Home > Library > Health > Psychoanalysis Dictionary
The notion of amnesia is of neuropathological origin, but for Freud it was not functional defect in the registering of memories. Rather, he looked upon amnesia as a symptom resulting from repression, as a phenomenon which could be circumscribed but which was not a defense mechanism. He compared infantile amnesia to hysterical amnesia, of which in his view it was the forerunner, both forms being connected with the child's sexuality and Oedipus complex. Amnesia concealed mnemic traces of traumatic events and, more generally, contents of the unconscious. (When defined by Freud simply as the normal "fading of memories," [1893a, p. 9] by contrast, the idea of amnesia belonged to the psychology of consciousness rather than to the metapsychology of the unconscious.)
Amnesia was not a psychoanalytical discovery, but, beginning with his earliest psychoanalytical writings, notably the Studies on Hysteria (1895d), Freud interpreted it in terms of repression; in the ThreeEssays on the Theory of Sexuality (1905d), he extended the discussion to infantile amnesia.
In the development of Freud's thought, it was the neuropathological idea of amnesia that showed the way to his formulation of repression, even though, structurally speaking, amnesia was a result of repression. The phenomenon of the absence of a memory prompted Freud to posit the existence of an unconscious mnemic trace. Since he did not consider amnesia to be a defense mechanism, he sought to account for it in another way, namely by the mechanism of repression. Thus in the Three Essays, comparing infantile amnesia to the hysterical amnesia that he felt it foreshadowed, he saw both as the outcome of the repression of sexuality, especially childhood sexuality, which he described as polymorphously perverse ("Neuroses are, so to say, the negative of perversions." [p. 165]).
The patient was "genuinely unable to recollect" the "event which provoked the first occurrence, often many years earlier, of the phenomenon in question," which is why it was necessary "to arouse his memories under hypnosis of the time at which the symptom made its first appearance" (1893a, p. 3). The lifting of amnesia was the precondition of the cathartic abreaction of the affects bound to the trauma, the memory of which had been effaced: this was Freud's first theory of the neuroses, namely the theory of the traumatic causality of hysteria.
Amnesia, however, did not in this view succeed in completely wiping out the memory of the trauma, for patients suffered from obsessions, from hallucinatory visions, from what seemed like foreign bodies within their psyches. So long as no abreaction of affects took place, a struggle continued to rage between amnesia and hysterical obsessions, giving rise to "hypnoid states" of a consciousness riven by conflict. Such states might range, according to the strength of the repression, from "complete recollection to total amnesia" (1893a, p. 12). In this light, amnesia could be seen as the ultimate outcome of that defense by means of the "dissociation of groups of ideas" which until 1900 Freud held to be typical of hysteria, and which later he described as the result of repression (an adumbration of the notion of splitting might also be discerned here).
In The Interpretation of Dreams, Freud argued that the forgetting of dreams was not "a special case of the amnesia attached to dissociated mental states," for in all cases "repression . . . is the cause both of the dissociations and the amnesia attaching to their psychical content" (1900a, p. 521). As Freud moved from the theory of traumatic hysteria to the theory of dreams, therefore, his conception of amnesia evolved from dissociative splitting to repression.
It was on the basis of the durability of the impression attached to the trauma (concealed by amnesia but finding expression in symptoms) that Freud hypothesized the existence of an indestructible unconscious mnemic trace, which helps us understand how, to begin with, he had conceived of the mnemic trace as a so-called "unconscious memory." The German term "Erinnerungsspur," whose literal meaning is "memory trace," covered both the (paradoxical) idea of an unconscious memory, which is to say a memory that has succumbed to amnesia, and the idea of an unconscious mnemic trace.
In 1900 Freud asserted that mnemic traces were indestructible; in 1895 he had observed that impressions associated with traumatic seductions preserved their sensory intensity and freshness when amnesia protected them from the wearing-away process that they would have undergone had they not been buried in the unconscious. By thus insisting upon the sensory vividness of what amnesia concealed, Freud depicted a quasi-hallucinatory mode of psychic representation consonant on the one hand with a post-traumatic accentuation of impressions that led in particular to the constitution of "mnemic symbols," and, on the other hand, with his later theoretical claim that unconscious ideas were necessarily figurative in nature.
The notion of amnesia, though it cleared the way for the psychoanalytical notions of the unconscious and of repression, itself remained a phenomenological idea belonging to descriptive psychopathology and marked by the idea of deficiency even if it went beyond it. While amnesia certainly meant a contraction of conscious memory that was not attributable to any functional deficiency of mnemonic fixation, it nonetheless implied a diminution of the capacities of the ego. The forgetting imposed by amnesia (for it was not intentional) was the effect of a defense mechanism that was itself unconscious, namely repression. Such forgetting was experienced, painfully, as consciousness of a repression either under way or already completed; and amnesia could also be the outcome of defense mechanisms other than repression (projection, splitting, foreclosure).
Since new repressions are always in the making, remembering does not make it possible to lift the amnesia completely. In "Constructions in Analysis" (1937d), Freud used the same terminology as in 1895 or 1900, but his standpoint had changed. He continued to think, to be sure, that the aim of analysis, starting, say, from "fragments of [the patient's] memories in his dreams" (p. 258), was to induce remembering, to lift amnesia. But he now felt that this procedure could never be total and that it could not even be embarked upon unless repetitionnotably the manifestation of affective impulses in the transferencewas taken into account. Inasmuch as amnesia continued to obscure entire aspects of the past, it was impossible ever to reconstitute that past in its entirety, and the analyst must be content to (re)construct it on the basis of what took place during analysis. This is not to say that Freud abandoned his fundamental historical perspective and embraced fictions, but simply that he redefined interpretation, independently of amnesia and its removal, as "probable historical truth" (p. 261).
This "probable" truth, as opposed to the whole truth, belongs to the episteme of modern history. How can the correctness of a construction be proved? One aspect of such a proof is connected to the set of problems surrounding amnesia and its lifting: communicating an accurate construction to the analysand may on occasion cause a temporary aggravation of the symptoms and the production of "lively recollections . . . described [by the patient] as 'ultra-clear"' and involving not "the subject of the construction but details relating to that subject" (p. 266).
Infantile prehistory, when the infant can barely speak, was in Freud's view affected by amnesia in a very particular way, and amnesias coming into play in later years, including hysterical amnesia, were derived from this primary structural amnesia, the concept of which brought Freud close to the idea of primal repression. What appeared as amnesia was indeed sometimes attributable to primal repression. In "'A Child Is Being Beaten"' (1919e), analyzing an infantile beating-fantasy, Freud emphasized, apropos of its most important phase (being beaten by the father), that "it has never had a real existence. It is never remembered, it has never succeeded in becoming conscious. It is a construction of analysis, but it is no less a necessity on that account" (p. 185). Here amnesia affects not a forgotten event but rather a fantasy about which there is no necessity to claim that it was at one time conscious. In such cases the amnesia could be removed only partially, as for example when "an elaborate superstructure of day-dreams" (p. 190) represented the fantasy in an indirect way. Here at last the notion of amnesia was completely absorbed by that of repression.
As noted above, "amnesia" is a term belonging to phenomenological psychopathology rather than to psychoanalysis: it refers to the symptom rather than the cause, and it connotes a lack (a-mnesia), which places it close to ideas of deficit. With respect to the psychology of consciousness, it points up the existence of the unconscious in one of its most spectacular effects. But if it opens the door to the metapsychological ideas of mnemic traces and repression, its affiliation with phenomenological psychopathology and cognitive psychology means that it belongs at once to several disciplines: amnesia is involved with the mnemonic "recalling" of information concerning a traumatic area, but a psychogenic causality does not exclude a cognitive or neurophysiological one.
Finally, since amnesia is centered entirely on a reduction of conscious memory, it is not compatible with the later developments in Freud's thinking on constructions in analysis, although it is true that the accuracy of a construction may bring about the removal of amnesiathus tending to confirm that Freud never completely abandoned the theory of traumatic seduction and the amnesia to which such a seduction gave rise. In "Remembering, Repeating and Working-Through" (1914g), Freud argued that the "fabric of the neurosis" itself provided "compelling evidence" for the reality of events experienced by the subject "in very early childhood and . . . not understood at the time" (p. 149); in other words, neither the lifting of amnesia nor even a reconstruction of the past was required-a proposition that amounts to a radical refutation of any "verificationist" epistemology. Psychoanalysis is concerned with historical truth, with infantile and psychic realities lying on a different plane, ontologically speaking, from amnesia and that which amnesia conceals, even if the latter can indeed show us the way to the former.
Bibliography
Freud, Sigmund. (1900a). The interpretation of dreams. SE, 4-5.
. (1905d). Three essays on the theory of sexuality. SE, 7: 123-243.
. (1914g). Remembering, repeating and working-through (Further recommendations on the technique of psycho-analysis, II). SE, 12: 145-156.
. (1919e). 'A child is being beaten': a contribution to the study of the origin of sexual perversions. SE, 17: 175-204.
. (1937d). Constructions in analysis. SE, 23: 255-269.
Freud, Sigmund, and Breuer, Josef. (1893a). On the psychical mechanism of hysterical phenomena: preliminary communication. SE, 2: 1-17.
Further Reading
Trewartha, M. (1990). On postanalytic amnesia. Annual of Psychoanalysis, 18, 153-174.
Wetzler, S. and Sweeney, J. (1986). Childhood amnesia: a cognitive-psychological conceptualization. Journal of the American Psychoanalytic Association, 34, 663-686.
FRAN?OIS RICHARD
Oxford Companion to the Mind:
amnesia Top
Home > Library > Health > World of the Mind
The popular conception of amnesia is probably typified by the occasional newspaper report of the appearance of someone who has mysteriously lost his memory. The person has no idea what his name is, where he comes from, or indeed about any of his past. Such cases usually recover their memory within a day or two, and typically turn out to be people attempting to escape from some socially stressful situation by simply opting out through the mechanism of dissociation. The precise nature of their memory defect is variable and seems to depend very much on their own views about how the human memory system works. In this respect they resemble hysterical patients suffering from glove anaesthesia, numbness in the hand which extends up to the wrist but not beyond and bears no relationship to the underlying pattern of innervation of the hand, indicating that it is of psychogenic origin rather than based on a physiological defect. The extent to which psychogenic amnesia represents genuine inability to recall, as opposed to conscious refusal to remember, is hard to ascertain. For further details see Pratt (in Whitty and Zangwill 1977).
The most extensively studied form of amnesia is that resulting from damage to the limbic system of the brain, typically involving the temporal lobes, hippocampus, and mamillary bodies. Such damage may occur in people suffering from Korsakoff syndrome, which results from a prolonged period of drinking too much alcohol and eating too little food, leading to a vitamin deficiency of thiamine (vitamin B1). Such patients often go through a delirious confused state, before stabilizing. They may then show a range of symptoms extending from considerable general intellectual impairment with relatively little memory decrement to occasional cases in which a relatively pure memory defect occurs. A broadly comparable memory defect occasionally occurs following encephalitis, and may also be produced by other kinds of brain damage such as stroke, tumour, or coal gas poisoning. There is some controversy over whether such a wide range of patients have a common memory defect, or whether subtle differences occur but the broad pattern of symptoms is similar.
Such patients have no difficulty in knowing where they grew up or telling you about their job or family background. In the case of relatively pure amnesics at least, their ability to use language is unimpaired, as is their general knowledge of the world. Their short-term memory also appears to be intact, at least in many cases. Their ability to repeat back a telephone number is just as good as would be the case in a normal person, and if you present them with a list of words, they show the normal tendency for the last few words presented to be well recalled. Their retention of the earlier words in a list is, however, likely to be very poor indeed.
The amnesic defect in the case of these patients appears to be one of episodic memory. They would be quite unable to tell you what they had for breakfast, and would very probably have no idea where they were or how long they had been there. If you had spent the morning testing them, by the afternoon they would probably fail to recognize you, and if asked for items of current information such as the name of the prime minister, would be likely to come up with a totally inappropriate response, naming a figure from twenty or thirty years ago. They have great difficulty in learning lists of words, whether you test them by recall or recognition, and have similar problems in remembering non-verbal material such as pictures of faces or objects.
There are, however, aspects of long-term memory that seem to be relatively unimpaired. Amnesic patients can learn motor skills, and one case, a pianist who was taught a tune on one day, had no difficulty in reproducing it on another. But characteristically such patients have no idea how or when they acquired the relevant information. A classic example is that cited by the Swiss psychologist Claparde, who on one occasion secreted a pin in his hand before shaking hands with an amnesic patient. On a subsequent day when he extended his hand the patient withdrew hers. When asked why, she could give no justification other than the general comment that sometimes things were hidden in people's hands. As one would expect from this demonstration, amnesics appear to be quite capable of classical avoidance conditioning. They are also quite capable of learning verbal materials under certain conditions. For example, Warrington and Weiskrantz used a learning procedure whereby subjects were presented with a series of words, and recall was tested by presenting the first three letters of each word and requiring the subject to produce the whole word. When tested in this way, amnesics were virtually normal.
What characterizes the long-term learning tasks that amnesics can do? This is still a controversial issue, but broadly speaking the tasks seem to be ones in which the patient simply has to use the information available in his memory store, without needing to worry about how it was acquired. The case where he is cued by being presented with the initial letters may be interpreted as simply a problem-solving task where he must find a word that fits these particular constraints. Having recently been presented with the relevant word will in fact make it more available, but he does not need to know this in order to take advantage of such an effect.
While classic amnesics like those just described are theoretically extremely interesting, patients having such a dense amnesia unaccompanied by more general intellectual deterioration are relatively rare. It is much more common for memory disturbance to stem from the after-effects of a blow on the head, as is often the case in road traffic accidents. Consider, for example, a motorcyclist who is involved in an accident causing a severe head injury. He is likely to lose consciousness for a period which may range from a few seconds to several months; if and when he regains consciousness he is likely to show a range of memory problems. It is usual to distinguish three separate types or aspects of such traumatic amnesia, namely retrograde amnesia, post-traumatic amnesia, and anterograde amnesia.
On recovery there will be evidence of loss of memory extending over the period between the injury and full return of consciousness. Following a head injury there will be a period of confusion characterized by the patient's inability to orient himself in time and place. The duration of post-traumatic amnesia, which will comprise the duration of total and partial loss of consciousness, provides a useful measure of the severity of the patient's injury and so permits some estimate of the extent of probable recovery to be made. On emerging from post-traumatic amnesia the patient is still likely to show considerable retrograde amnesia. This is indicated by an inability to remember events before the accident. In the case of a severe blow the amnesia may extend over a period of several years. Typically this blank period becomes less and less, with earlier memories being recovered first, although the process is far from systematic, with 'islands' of memory cropping up in periods that are otherwise still blank. Typically the retrograde amnesia shrinks up to a point within a few minutes of the accident. These final few moments are seldom ever recovered, possibly because the memory trace was never adequately consolidated. This point was illustrated rather neatly in a study of American football players who had been 'dinged' (concussed) during a game. As they were led off the field they were asked the code name of the play in which they had been engaged when concussed (e.g. 'Thirty-two pop'). Typically they were able to supply this information immediately on leaving the field, but when retested 20 to 30 minutes later they were quite unable to provide it. A subsequent study showed that this was not simply due to normal forgetting, or to the mnemonic limitations of American football players, but suggests that failure of memory traces to consolidate during the concussed state may be an important factor.
The third memory disturbance associated with head injury concerns difficulty in learning and retaining new information. During the process of recovery from a closed head injury, memory problems are commonly reported, together with difficulties in concentrating and a tendency to become fatigued much more rapidly than was previously the case. While the memory problems of patients with head injuries have been rather less extensively investigated than those of the classic amnesic syndrome, we do know that they show some of the same characteristics. Typically short-term memory is not greatly affected, and if one presents an amnesic head-injured patient with a list of words, he is likely to do reasonably well on the last few presented, but relatively poorly on the earlier items in the list. Although not much work has been done in directly comparing such patients with other types of amnesics, it seems likely that the pattern will be somewhat different, since closed head injury appears to cause neuronal and vascular damage in large areas of the brain as opposed to specific subcortical damage in the classic amnesic syndrome. Furthermore, whereas the classic amnesic patient does not completely recover, head-injured patients typically do improve quite substantially from the time when they emerge from their initial period of post-traumatic amnesia. In many cases they return to performing at what appears to be their level before injury.
Amnesia is an important component in senile and pre-senile dementia. In both these cases intellectual deterioration probably results from a substantial loss of cortical neurons, and in addition to showing memory problems such patients usually show a more general intellectual deterioration. This in turn increases the memory problem, since they seem unable or unwilling to use effective learning strategies.
We have so far discussed patients who have long-term learning problems but normal short-term memory. However, the reverse has also been reported. Tim Shallice and Elizabeth Warrington (1970) describe a patient who had great difficulty in repeating back sequences of numbers, the longest sequence he could repeat back reliably being two digits. He was, however, quite unimpaired in his long-term memory as measured both by his ability to learn word sequences and by his memory for faces and for the events of everyday life. As is suggested in its entry, short-term memory is almost certainly not a single unitary function, and there is some evidence to suggest that there are other patients who have different defects of the short-term memory system.
Theoretical interpretation of the various ways in which memory can break down obviously depends crucially on one's interpretation of normal memory. As such, amnesia presents a theoretically important though difficult question. We have in recent years made progress in exploring and defining more precisely the amnesic syndrome, but are as yet some way from constructing a completely adequate interpretation at a psychological, neurological, or biochemical level.
(Published 1987)
 Alan Baddeley
Bibliography
Baddeley, A. D. (1982). 'Amnesia as a minimal model and an interpretation'. In Cermak, L. S. (ed.), Human Memory and Amnesia.
Shallice, T., and Warrington, E. K. (1970). 'Independent functioning of the verbal memory stores: a neuropsychological study'. Quarterly Journal of Experimental Psychology, 22.
Whitty, C. W. M., and Zangwill, O. L. (eds.) (1977). Amnesia.
Word Tutor:
amnesia Top
Home > Library > Literature & Language > Word Tutor
IN BRIEF: Loss of memory.
He suffered from temporary amnesia after the accident and could not remember anything for a while.
LearnThatWord.com is a free vocabulary and spelling program where you only pay for results!
Dictionary of Cultural Literacy: Science:
amnesia Top
Home > Library > Science > Science Dictionary
(am-nee-zhuh)
A loss of memory, especially one brought on by some distressing or shocking experience.
A common variant is selective amnesia; the term is applied to public officials who, when questioned about alleged wrongdoing, profess that they cannot remember.
Mosby's Dental Dictionary:
amnesia Top
Home > Library > Health > Dental Dictionary
(amnz-?, -zh?)
n
The lack or loss of memory.
Random House Word Menu:
categories related to 'amnesiac' Top
Home > Library > Literature & Language > Word Menu Categories
For a list of words related to amnesiac, see:
Stupid, Ignorant, or Confused
Rhymes:
amnesic Top
Home > Library > Literature & Language > Rhymes
See words rhyming with "amnesic."
Bradford's Crossword Solver's Dictionary:
amnesia Top
Home > Library > Literature & Language > Crossword Clues
See crossword solutions for the clue Amnesia.
Wikipedia on Answers.com:
Amnesia Top
Home > Library > Miscellaneous > Wikipedia
For other uses, see Amnesia (disambiguation).
Not to be confused with memory loss.
Amnesia
Classification and external resources
ICD-10
F04, R41.3
ICD-9
294.0, 780.9, 780.93
MeSH
D000647
Amnesia (from Greek ?̦ͦǦ?) is a condition in which one's memory is lost. The causes of amnesia have traditionally been divided into categories. Functional causes are psychological factors, such as mental disorder, post-traumatic stress or, in psychoanalytic terms, defense mechanisms. Amnesia may also appear as spontaneous episodes, in the case of transient global amnesia.[1]
Anterograde amnesia, is the loss of short-term memory, the loss or impairment of the ability to form new memories through memorization. People may find themselves constantly forgetting a piece of information, people or events after a few seconds or minutes, because the data does not transfer successfully from their conscious short-term memory into permanent long-term memory.
Retrograde amnesia, the loss of pre-existing memories to conscious recollection, beyond an ordinary degree of forgetfulness. The person may be able to memorize new things that occur after the onset of amnesia (unlike in anterograde amnesia), but is unable to recall some or all of their life or identity prior to the onset.
However, there are different types of memory, for example procedural memory (i.e. automated skills) and declarative memory (personal episodes or abstract facts), and often only one type is impaired. For example, a person may forget the details of personal identity, but still retain a learned skill such as the ability to play the piano.
In addition, the terms are used to categorize patterns of symptoms rather than to indicate a particular cause (etiology). Both categories of amnesia can occur together in the same patient, and commonly result from drug effects or damage to the brain regions most closely associated with episodic memory: the medial temporal lobes and especially the hippocampus.
An example of mixed retrograde and anterograde amnesia may be a motorcyclist unable to recall driving his motorbike prior to his head injury (retrograde amnesia), nor can he recall the hospital ward where he is told he had conversations with family over the next two days (anterograde amnesia).
The effects of amnesia can last long after the condition has passed. Some sufferers claim that their amnesia changes from a neurological condition to also being a psychological condition, whereby they lose confidence and faith in their own memory and accounts of past events.
Another effect of some forms of amnesia may be impaired ability to imagine future events. A 2006 study showed that future experiences imagined by amnesiacs with bilaterally damaged hippocampus lacked spatial coherence, and the authors speculated that the hippocampus may bind different elements of experience together in the process of re-experiencing the past or imagining the future.[2]
Types and causes of amnesia
Post-traumatic amnesia is generally due to a head injury (e.g., a fall, a knock on the head). Traumatic amnesia is often transient, but may be permanent of 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.
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 refers to the inability to recall information, usually about stressful or traumatic events in persons' lives, such as a violent attack or rape. 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. This contrasts with e.g. anterograde amnesia caused by amnestics such as benzodiazepines or alcohol, where an experience was prevented from being transferred from temporary to permanent memory storage: it will never be recovered, because it was never stored in the first place. 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, unresolved and therefore may return. The Merck Manual defines it as "one or more episodes of amnesia in which the inability to recall some or all of one's past and either the loss of one's identity or the formation of a new identity occur with sudden, unexpected, purposeful travel away from home." [3] While popular in fiction, it is extremely rare.
Posthypnotic amnesia is where events during hypnosis are forgotten, or where past memories are unable to be recalled.
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
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 nor any other neurological deficits. The cause of this syndrome is not clear, hypotheses include transient reduced blood flow, possible seizure or an atypical type of migraine. Patients are typically amnestic of events more than a few minutes in the past, though immediate recall is usually preserved.
Source amnesia is a memory disorder in which someone can recall certain information, but they do not know where or how they obtained the information.
Memory distrust syndrome is a term invented by the psychologist Gisli Gudjonsson to describe a situation where someone is unable to trust their own memory.
Blackout phenomenon can be caused by excessive short-term alcohol consumption, with the amnesia being of the anterograde type.
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.
Drug-induced amnesia is intentionally caused by injection of an amnesiac 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.
Electroconvulsive therapy in which seizures are electrically induced in patients for therapeutic effect can have acute effects including both retrograde and anterograde amnesia.
Prosopamnesia is the inability to remember faces, even in the presence of intact facial recognition capabilities. Both acquired and inborn cases have been documented.
Situation-Specific amnesia can arise in a variety of circumstances (e.g., 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.
See also
Betrayal Trauma
Doug Bruce
Emotion and memory
False memory
HM (patient)
KC (patient)
Benjaman Kyle
Repressed memories
Mr. Nobody
Transient epileptic amnesia (TEA)
Clive Wearing
List of films featuring mental illness
References
Notes
^ eMedicine - Transient Global Amnesia : Article by Roy Sucholeiki
^ Patients with hippocampal amnesia cannot imagine new experiences, Proceedings of the National Academy of Sciences.
^ The Merck Manuals Online
Articles and topics related to Amnesia
v  d  eMental and behavioral disorders (F  290C319)
Neurological/symptomatic
Dementia
Mild cognitive impairment  Alzheimer's disease  Multi-infarct dementia  Pick's disease  CreutzfeldtCJakob disease  Huntington's disease  Parkinson's disease  AIDS dementia complex  Frontotemporal dementia  Sundowning, Wandering
Other
Delirium  Post-concussion syndrome  Organic brain syndrome
Psychoactive substances, substance abuse, drug abuse and substance-related disorders
Intoxication/Drug overdose  Physical dependence  Substance dependence  Rebound effect  Double rebound  Withdrawal
Schizophrenia, schizotypal and delusional
Psychosis (Schizoaffective disorder, Schizophreniform disorder, Brief reactive psychosis)  Schizophrenia (Disorganized schizophrenia, Delusional disorder, Folie  deux)
Mood (affective)
Mania  Bipolar disorder (Bipolar I, Bipolar II, Cyclothymia, Bipolar NOS)  Depression (Major depressive disorder, Dysthymia, Seasonal affective disorder, Atypical depression, Melancholic depression)
Neurotic, stress-related and somatoform
Anxiety disorder
Phobia
Agoraphobia  Social anxiety/Social phobia (Anthropophobia)  Specific phobia (Claustrophobia)  Specific social phobia
Other
Panic disorder/Panic attack  Generalized anxiety disorder  OCD  stress (Acute stress reaction, PTSD)
Adjustment disorder
Adjustment disorder with depressed mood
Somatoform disorder
Somatization disorder  Body dysmorphic disorder  Hypochondriasis  Nosophobia  Da Costa's syndrome  Psychalgia  Conversion disorder (Ganser syndrome, Globus pharyngis)  Neurasthenia  Mass Psychogenic Illness
Dissociative disorder
Dissociative identity disorder  Psychogenic amnesia  Fugue state  Depersonalization disorder
Physiological/physical behavioral
Eating disorder
Anorexia nervosa  Bulimia nervosa  Rumination syndrome  NOS
Nonorganic
sleep disorders
(Nonorganic hypersomnia, Nonorganic insomnia)  Parasomnia (REM behavior disorder, Night terror, Nightmare)
Sexual
dysfunction
sexual desire (Hypoactive sexual desire disorder, Hypersexuality)  sexual arousal (Female sexual arousal disorder)  Erectile dysfunction  orgasm (Anorgasmia, Delayed ejaculation, Premature ejaculation, Sexual anhedonia)  pain (Vaginismus, Dyspareunia)
Postnatal
Postpartum depression  Postnatal psychosis
Adult personality and behavior
Sexual and
gender identity
Sexual maturation disorder  Ego-dystonic sexual orientation  Sexual relationship disorder  Paraphilia (Voyeurism, Fetishism)
Other
Personality disorder  Impulse control disorder (Kleptomania, Trichotillomania, Pyromania, Dermatillomania)  Body-focused repetitive behavior  Factitious disorder (Mnchausen syndrome)
Mental disorders diagnosed in childhood
Mental retardation
X-Linked mental retardation (Lujan-Fryns syndrome)
Psychological development
(developmental disorder)
Specific  Pervasive
Emotional and behavioral
ADHD  Conduct disorder (ODD)  emotional disorder (Separation anxiety disorder)  social functioning (Selective mutism, RAD, DAD)  Tic disorder (Tourette syndrome)  Speech (Stuttering, Cluttering)  Movement disorder (Stereotypic)
Symptoms and uncategorized
Catatonia  False pregnancy  Intermittent explosive disorder  Psychomotor agitation  Sexual addiction  Stereotypy  Psychogenic non-epileptic seizures  Klver-Bucy syndrome
M: PSO/PSI
mepr
dsrd (o, p, m, p, a, d, s), sysi/epon, spvo
proc(eval/thrp), drug(N5A/5B/5C/6A/6B/6D)
v  d  eSymptoms and signs: cognition, perception, emotional state and behaviour (R40CR46, 780.0C780.5, 781.1)
Cognition
Alteration of
consciousness
Confusion (Delirium)  Somnolence  Obtundation  Stupor  Unconsciousness (Syncope, Coma, Persistent vegetative state)
Fainting/Syncope
Carotid sinus syncope ? Heat syncope ? Vasovagal episode
Other
Amnesia (Anterograde amnesia, Retrograde amnesia)  Dizziness (Vertigo, Presyncope/Lightheadedness, Disequilibrium)  Convulsion
Emotional state
Anxiety  Irritability  Hostility  Suicidal ideation
Behavior
Verbosity
Perception/
sensation
disorder
Olfaction : Anosmia  Hyposmia  Dysosmia  Parosmia  Hyperosmia
Taste: Ageusia  Hypogeusia  Dysgeusia  Parageusia  Hypergeusia
Hallucination: Auditory hallucination
M: PSO/PSI
mepr
dsrd (o, p, m, p, a, d, s), sysi/epon, spvo
proc(eval/thrp), drug(N5A/5B/5C/6A/6B/6D)
M: OLF
anat, recp
sysi
-
M: TST
anat, phys
sysi
-
v  d  eMemory
Basic concepts
Encoding ? Storage ? Recall
Attention ? Memory consolidation ? Neuroanatomy of memory
Long-term memory
Active recall ? Autobiographical memory ? Declarative memory ? Episodic memory ? Explicit memory ? Flashbulb memory ? Hyperthymesia ? Implicit memory ? Procedural memory ? Rote learning ? Selective retention ? Semantic memory ? Tip of the tongue
Short-term memory
"The Magical Number Seven, Plus or Minus Two" ? Working memory
Sensory memory
Echoic memory ? Eidetic memory ? Iconic memory ? Motor learning ? Visual memory
Forgetting
Amnesia ? Anterograde amnesia ? Childhood amnesia ? Decay theory ? Forgetting curve ? Interference theory ? Memory inhibition ? Motivated forgetting ? Post-traumatic amnesia ? Psychogenic amnesia ? Repressed memory ? Retrograde amnesia ? Selective memory loss ? Transient global amnesia ? Weapon focus
Research
Art of memory ? Memory and aging ? Exceptional memory ? Indirect tests of memory ? Lost in the mall technique ? Memory disorder ? Methods used to study memory ? Reconstruction of automobile destruction ? The Seven Sins of Memory
Related concepts
Absent-mindedness ? AtkinsonCShiffrin memory model ? Confabulation ? Context-dependent memory ? Cryptomnesia ? Effect of Alcohol on Memory ? Emotion and memory ? Exosomatic memory ? Flashbacks ? Free recall ? Involuntary memory ? Levels-of-processing effect ? List of memory biases ? Memory and aging ? Memory for the future ? Memory and trauma ? Metamemory ? Mnemonic ? Muscle memory ? Priming ? Prospective memory ? Recovered memory therapy ? Retrospective memory ? Sleep and Memory ? Source-monitoring error ? Memory improvement
Culture and society
Cultural memory ? False memory syndrome ? Politics of memory ? Shass Pollak ? Transactive memory ? Memory and social interactions ? Memory sport ? World Memory Championships
Notable people
Robert A. Bjork ? Stephen J. Ceci ? Susan Clancy ? Hermann Ebbinghaus ? Sigmund Freud ? Patricia Goldman-Rakic ? Jonathan Hancock ? Judith Lewis Herman ? HM (patient) ? Ivan Izquierdo ? Marcia K. Johnson ? Eric Kandel ? KC (patient) ? Elizabeth Loftus ? Geoffrey Loftus ? James McGaugh ? Paul R. McHugh ? George Armitage Miller ? Brenda Milner ? Lynn Nadel ? Dominic O'Brien ? Ben Pridmore ? Henry L. Roediger III ? Steven Rose ? Cosmos Rossellius ? Daniel Schacter ? Richard Shiffrin ? Arthur P. Shimamura ? Andriy Slyusarchuk ? Larry Squire ? Susumu Tonegawa ? Anne Treisman ? Endel Tulving ? Robert Stickgold
This entry is from Wikipedia, the leading user-contributed encyclopedia. It may not have been reviewed by professional editors (see full disclaimer)
Donate to Wikimedia
Translations:
Amnesia Top
Home > Library > Literature & Language > Translations
Dansk (Danish)
n. - amnesi, hukommelsestab
Nederlands (Dutch)
(gedeeltelijk) geheugenverlies
Fran?ais (French)
n. - amnsie
Deutsch (German)
n. - Ged?chtnisschwund, Amnesie
˦˦Ǧͦɦ? (Greek)
n. - (ЦȦϦ., ̦Ӧ.) ̦ͦǦ?
Italiano (Italian)
amnesia
Portugus (Portuguese)
n. - amnsia (f) (Psicol.) (Med.)
ܧڧ (Russian)
ѧާߧ֧٧ڧ, ֧ ѧާ
Espa?ol (Spanish)
n. - amnesia
Svenska (Swedish)
n. - minnesf?rlust
ģ壩(Chinese (Simplified))
ȱʧ, ֢
ģw(Chinese (Traditional))
n. - ӛȱʧ, ֢
??? (Korean)
n. - ???, ????
ձZ (Japanese)
n. - , ֢, ӛʧ
??????? (Arabic)
?(?????) ????? ??????? ???? ???
????? (Hebrew)
n. - ????? ?????, ??????, ?????
If you are unable to view some languages clearly, click here.
To select your translation preferences click here.
\n"; for(i=0; i < radlinks.length; ++i) { html += "" + radlinks[i].term + "\n"; } html += "\n"; var obj = document.getElementById('top_radlinks'); if(obj!=null){ obj.innerHTML = html; obj.style.display='block'; } } google_ad_client = 'ca-gurunet_radlinks_js'; google_ad_channel = 'link-definitions-3 RA_LUhealth RA_LUUS'; google_ad_output = 'js'; google_max_num_ads = '0'; google_language = 'en'; google_encoding = 'utf-8'; google_hints = ''; google_safe = 'medium'; google_adtest = 'off'; google_num_radlinks = '4'; google_max_radlink_len = '25'; google_rl_filtering = 'high'; google_rl_mode = 'relevance';
Related topics:
amnesiphobia
mind
amnesiac
Related answers:
What do you lose when you have amnesia? Read answer...
How do you remember when you have amnesia? Read answer...
What can one do to get amnesia? Read answer...
Help us answer these:
Four characteristics that differentiate organic amnesia from dissociative amnesia?
What is the mechanism of amnesia?
How do you treat amnesia?
Post a question - any question - to the WikiAnswers community:
Copyrights:
American Heritage Dictionary. The American Heritage? Dictionary of the English Language, Fourth Edition Copyright ? 2007, 2000 by Houghton Mifflin Company. Updated in 2009. Published by Houghton Mifflin Company. All rights reserved. Read more
Britannica Concise Encyclopedia. Britannica Concise Encyclopedia. ? 1994-2011 Encyclop?dia Britannica, Inc. All rights reserved. Read more
McGraw-Hill Science & Technology Encyclopedia. McGraw-Hill Encyclopedia of Science and Technology. Copyright ? 2005 by The McGraw-Hill Companies, Inc. All rights reserved. Read more
Oxford Companion to the Body. The Oxford Companion to the Body. Copyright ? 2001, 2003 by Oxford University Press. All rights reserved. Read more
Oxford Dictionary of Sports Science & Medicine. The Oxford Dictionary of Sports Science & Medicine. Copyright ? Michael Kent 1998, 2006, 2007. All rights reserved. Read more
Columbia Encyclopedia. The Columbia Electronic Encyclopedia, Sixth Edition Copyright ? 2011, Columbia University Press. Licensed from Columbia University Press. All rights reserved. www.cc.columbia.edu/cu/cup/. Read more
Gale Dictionary of Psychoanalysis. International Dictionary of Psychoanalysis. Copyright ? 2005 by The Gale Group, Inc. All rights reserved. Read more
Oxford Companion to the Mind. The Oxford Companion to the Mind. Second Edition. Copyright ? Oxford University Press, 2004. All rights reserved. Read more
Word Tutor. Copyright ? 2004-present by eSpindle Learning, a 501(c) nonprofit organization. All rights reserved.
eSpindle provides personalized spelling and vocabulary tutoring online; sign up free. Read more
Dictionary of Cultural Literacy: Science. The New Dictionary of Cultural Literacy, Third Edition Edited by E.D. Hirsch, Jr., Joseph F. Kett, and James Trefil. Copyright ? 2002 by Houghton Mifflin Company. Published by Houghton Mifflin. All rights reserved. Read more
Mosby's Dental Dictionary. Mosby's Dental Dictionary. Copyright ? 2004 by Elsevier, Inc. All rights reserved. Read more
Random House Word Menu. ? 2010 Write Brothers Inc. Word Menu is a registered trademark of the Estate of Stephen Glazier. Write Brothers Inc. All rights reserved. Read more
Rhymes. Oxford University Press. ? 2006, 2007 All rights reserved. Read more
Bradford's Crossword Solver's Dictionary. Collins Bradford's Crossword Solver's Dictionary ? Anne Bradford, 1986, 1993, 1997, 2000, 2003, 2005, 2008 HarperCollins Publishers All rights reserved. Read more
Wikipedia on Answers.com. This article is licensed under the Creative Commons Attribution/Share-Alike License. It uses material from the Wikipedia article Amnesia. Read more
Translations. Copyright ? 2007, WizCom Technologies Ltd. All rights reserved. Read more
Related answers
How do you get amnesia?
What is amnesia?
Amnesia is a loss of what?
Can cats get amnesia?
What are symptoms of amnesia?
What is TM Amnesia? ? More
Answer these
Is blood amnesia same as amnesia?
What is the Difference between amnesia and dissociative amnesia?
How was amnesia discovered? ? More
Featured guides
Best Junk Removal Services
How To Buy An Extended Auto Warranty
How To Care For Your Cell Phone Battery
Best Cell Phone Accessories Wholesale
How to Build a Brick Oven for Pizza
Follow us
Facebook
Twitter
YouTube
Mentioned in
amnesiphobia
mind
amnesiac
chemamnesia
amnestic
memory
retrograde amnesia
posttraumatic
Guare, John (Quotes By)
infonesia
internesia
amnesic
The Lady Forgets (1989 Drama Film)
The Missing 24 Hours (1976 Crime Film)
? More? More
Related topics
brain
cerebral cortex
hypothalamus
limbic system
memory
Black Hole
Claims of Psychoanalysis to Scientific Interest
Forgetting
Infantile Amnesia
Lifting of Amnesia
Memory
Mnemic Symbol
Mnemic Trace/Memory Trace
Psychoanalytic Treatment
Remembering
Reminiscence
Repression? More
Site
Sitemap
ReferenceAnswers
WikiAnswers
VideoAnswers
Coupons
Guides
Company
About
Jobs
Press
Legal
Terms of Use
Privacy Policy
IP Issues
Disclaimer
Tools
1-Click Answers
AnswerTips
Webmasters
Apps/Add-ons
Community
Guidelines
Reputation
Roles
Help
Updates
Email
Watchlist
RSS
Blog
International Sites English Deutsch Espa?ol Fran?ais Italiano Tagalog
Copyright ? 2011 Answers Corporation
"); }
