AMNESIA

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 repetition—notably the manifestation of affective impulses in the transference—was 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 amnesia—thus 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.

FranÇois Richard

See also: 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.

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.

Amnesia

How amnesia is manifested

Causes of amnesia

Resources

Amnesia is a dissociative psychological disorder manifested by total or partial loss of memory and usually caused by a trauma. Unlike ordinary forgetfulness (the inability to remember a friend’s telephone number), amnesia is a serious threat to a person’s professional and social life. Amnesia, which depending on its cause can be either organic and psychogenic, has several types.

How amnesia is manifested

Global or generalized amnesia indicates the total loss of a person’s identity: the individual has forgotten who she or he is. What makes this type of amnesia baffling is the fact that only personal memory is affected. The amnesiac does not remember who he or she is but displays no loss of general knowledge. A person suffering from retrograde amnesia cannot remember events that happened immediately before the trauma. In anterograde amnesia, all events following the trauma are forgotten. Finally, amnesia can also be selective, or categorical, manifested by a person’s inability to remember events related to a specific incident.

Causes of amnesia

The causes of amnesia can be physiological and/or psychological. Amnesia caused by physical trauma is called organic amnesia, while the term psychogenic amnesia is used in reference to amnesia caused by psychological trauma.

Organic amnesia

Examples of organic amnesia include cases of memory loss following head injuries, brain lesions, stroke, substance abuse, carbon monoxide poisoning, malnutrition, electro-convulsive therapy, surgery, and infections. Persons suffering from any kind of organic amnesia display a number of typical characteristics. Their memory loss is anterograde: events after the trauma are forgotten. In addition, they can remember the distant past well, but their grasp of the immediate past is tenuous. If treatment is unsuccessful, the amnesiac’s condition can worsen, leading to progressive memory loss. In such cases, memory loss is irreversible. If therapy is successful, the patient may partially regain memories blocked by retrograde amnesia, while anterograde amnesia usually remains.

Psychogenic amnesia

The causes of psychogenic amnesia are psychological, and they include career-related stress, economic hardship, and emotional distress. Experts have maintained that psychogenic amnesia has no physiological causes, although recent research has established that emotional trauma may alter the brain physiology, thus setting the stage for the interplay of psychological and physiological factors in the etiology of amnesia. In other words, psychogenic amnesia may have secondary causes that could be defined as organic. The most enigmatic psychogenic amnesia is identity loss; the person affected by this type of amnesia loses all personal memories, while retaining his or her general (impersonal) knowledge. For example, the amnesiac may not know his or her name, but can still be able to speak an acquired second language. Furthermore, in psychogenic amnesia, there is no anterograde memory loss. Finally, although psychogenic amnesia is reversible and can end within hours or days, it is a serious condition that can be difficult to treat.

Diagnosis

In diagnosing amnesia, doctors look at several factors. During a physical examination, the doctor inquires about recent traumas or illnesses, drug and medication history, and checks the patient’s general health. Psychological exams may be ordered to determine the extent of amnesia and the memory system affected. The doctor may also order imaging tests such as magnetic resonance imaging (MRI) to reveal whether the brain has been damaged, and blood work to exclude treatable metabolic causes or chemical imbalances.

Treatment depends on the root cause of amnesia and is handled on an individual basis. Regardless of cause, cognitive rehabilitation may be helpful in learning strategies to cope with memory impairment.

Some types of amnesia, such as transient global amnesia, are completely resolved and there is no permanent loss of memory. Others, such as Korsakoff syndrome, associated with prolonged alcohol abuse or amnesias caused by severe brain injury, may be permanent. Depending on the degree of amnesia and its cause, victims may be able to lead relatively normal lives. Amnesiacs can learn through therapy to rely on other memory systems to compensate for what is lost.

Amnesia is only preventable in so far as brain injury can be prevented or minimized. Common sense approaches include wearing a helmet when bicycling or participating in potentially dangerous sports, using automobile seat belts, and avoiding excessive alcohol or drug use. Brain infections should be treated swiftly and aggressively to minimize the damage due to swelling. Victims of strokes, brain aneurysms, and transient ischemic attacks should seek immediate medical treatment.

KEY TERMS

Dissociative disorder— Referring to psychological conditions, such as psychogenic amnesia and multiple personality disorder, in which an area of personal memory is dissociated from a person’s consciousness.

Etiology— The cause or origin of a disease or condition.

Resources

BOOKS

Baddeley, Alan D., Michael D. Kopelman, and Barbara A. Wilson, eds. The Essential Handbook of Memory Disorders for Clinicians. Chichester, UK, and Hoboken, NJ: John Wiley, 2004.

Bowers, Jeffrey S., and Chad J. Marsolek. Rethinking Implicit Memory. Oxford, UK, and New York: Oxford University Press, 2003.

Carr, Alan. Abnormal Psychology. Hove, UK, and Philadelphia, PA: Psychology Press, 2001.

Papanicolaou, Andrew C. The Amnesias: A Clinical Textbook of Memory Disorders. Oxford, UK, and New York: Oxford University Press, 2006.

Schacter, Daniel L. The Seven Sins of Memory: How the Mind Forgets and Remembers. Boston, MA: Houghton Mifflin, 2002.

Squire, Larry R. and Daniel L. Schacter, eds. Neuropsychology of Memory. New York: Guilford, 2002.

PERIODICALS

Cipolotti, L. “Long-term Retrograde Amnesia.” Neurocase 8, no. 3 (2002): 177.

Cohen, N.J. “Amnesia is A Deficit in Relational Memory.” Psychological Science 11, no.6 (2001): 454-461.

Golden, Frederic. “Mental Illness: Probing the Chemistry of the Brain.” Time 157 (January 2001).

Knowlton, B.J. “Retrograde Amnesia.” Hippocampus 11, no. 1 (2001): 50-55.

Zoran Minderovic

Amnesia

Definition

Amnesia refers to the loss of memory. Memory loss may result from two-sided (bilateral) damage to parts of the brain vital for memory storage, processing, or recall (the limbic system, including the hippocampus in the medial temporal lobe).

Description

Amnesia can be a symptom of several neurodegenerative diseases; however, people whose primary symptom is memory loss (amnesiacs), typically remain lucid and retain their sense of self. They may even be aware that they suffer from a memory disorder.

People who experience amnesia have been instrumental in helping brain researchers determine how the brain processes memory. Until the early 1970s, researchers viewed memory as a single entity. Memory of new experiences, motor skills, past events, and previous conditioning were grouped together in one system that relied on a specific area of the brain.

If all memory were stored in the same way, it would be reasonable to deduce that damage to the specific brain area would cause complete memory loss. However, studies of amnesiacs counter that theory. Such research demonstrates that the brain has multiple systems for processing, storing, and drawing on memory.

Causes and symptoms

Amnesia has several root causes. Most are traceable to brain injury related to physical trauma, disease, infection, drug and alcohol abuse, or reduced blood flow to the brain (vascular insufficiency). In Wernicke-Korsakoff syndrome, for example, damage to the memory centers of the brain results from the use of alcohol or malnutrition. Infections that damage brain tissue, including encephalitis and herpes, can also cause amnesia. If the amnesia is thought to be of psychological origin, it is termed psychogenic.

There are at least three general types of amnesia:

• Anterograde. This form of amnesia follows brain trauma and is characterized by the inability to remember new information. Recent experiences and short-term memory disappear, but victims can recall events prior to the trauma with clarity.
• Retrograde. In some ways, this form of amnesia is the opposite of anterograde amnesia: the victim can recall events that occurred after a trauma, but cannot remember previously familiar information or the events preceding the trauma.
• Transient global amnesia. This type of amnesia has no consistently identifiable cause, but researchers have suggested that migraines or transient ischemic attacks may be the trigger. (A transient ischemic attack, sometimes called "a small stroke," occurs when a blockage in an artery temporarily blocks off blood supply to part of the brain.) A victim experiences sudden confusion and forgetfulness. Attacks can be as brief as 30-60 minutes or can last up to 24 hours. In severe attacks, a person is completely disoriented and may experience retrograde amnesia that extends back several years. While very frightening for the patient, transient global amnesia generally has an excellent prognosis for recovery.

Diagnosis

In diagnosing amnesia and its cause, doctors look at several factors. During a physical examination, the doctor inquires about recent traumas or illnesses, drug and medication history, and checks the patient's general health. Psychological exams may be ordered to determine the extent of amnesia and the memory system affected. The doctor may also order imaging tests such as magnetic resonance imaging (MRI) to reveal whether the brain has been damaged, and blood work to exclude treatable metabolic causes or chemical imbalances.

Treatment

Treatment depends on the root cause of amnesia and is handled on an individual basis. Regardless of cause, cognitive rehabilitation may be helpful in learning strategies to cope with memory impairment.

Prognosis

Some types of amnesia, such as transient global amnesia, are completely resolved and there is no permanent loss of memory. Others, such as Korsakoff syndrome, associated with prolonged alcohol abuse or amnesias caused by severe brain injury, may be permanent. Depending on the degree of amnesia and its cause, victims may be able to lead relatively normal lives. Amnesiacs can learn through therapy to rely on other memory systems to compensate for what is lost.

Prevention

Amnesia is only preventable in so far as brain injury can be prevented or minimized. Common sense approaches include wearing a helmet when bicycling or participating in potentially dangerous sports, using automobile seat belts, and avoiding excessive alcohol or drug use. Brain infections should be treated swiftly and aggressively to minimize the damage due to swelling. Victims of strokes, brain aneurysms, and transient ischemic attacks should seek immediate medical treatment.

Resources

PERIODICALS

Squire, Larry R., and Stuart M. Zola. "Amnesia, Memory and Brain Systems." Philosophical Transactions of the Royal Society of London, Series B 352 (1997): 1663.

KEY TERMS

Classical conditioning— The memory system that links perceptual information to the proper motor response. For example, Ivan Pavlov conditioned a dog to salivate when a bell was rung.

Emotional conditioning— The memory system that links perceptual information to an emotional response. For example, spotting a friend in a crowd causes a person to feel happy.

Explicit memory— Conscious recall of facts and events that is classified into episodic memory (involves time and place) and semantic memory (does not involve time and place). For example, an amnesiac may remember he has a wife (semantic memory), but cannot recall his last conversation with her (episodic memory).

Limbic system— The brain structures involved in memory.

Magnetic resonance imaging (MRI)— MRI uses a large circular magnet and radio waves to generate signals from atoms in the body. These signals are used to construct images of internal structures.

Motor skill learning— This memory system is associated with physical movement and activity. For example, learning to swim is initially difficult, but once an efficient stroke is learned, it requires little conscious effort.

Neurodegenerative disease— A disease in which the nervous system progressively and irreversibly deteriorates.

Priming memory— The memory system that joins perceptual and conceptual representations.

Transient ischemic attack— A sudden and brief blockage of blood flow in the brain.

Working memory— The memory system that relates to the task at hand and coordinates recall of memories necessary to complete it.

amnesia 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.

Amnesia

Definition

Description

Definition

Amnesia is a partial or total loss of memory.

Description

There are numerous causes of amnesia, including stroke, injury to the brain, surgery, alcoholism, encephalitis (inflammation of the brain), and electroconvulsive therapy. (Electroconvulsive therapy, or ECT, is a treatment for various mental disorders in which electricity is sent to the brain through electrodes.)

Contrary to the popular notion of amnesia—in which a person suffers a severe blow to the head, for example, and cannot recall his or her past life and experiences—the principal symptom of amnesia is the inability to retain new information, beginning at the point at which the amnesia began. The capacity to recall past experiences may vary, depending on the severity of the amnesia.

There are two types of amnesia: retrograde and anterograde. Retrograde amnesia refers to the loss of memory of one’s past and can vary from person to person. Some sufferers retain virtually full recall of things that happened prior to the onset of amnesia; others forget only their recent past, and still others lose all memory of their past lives. Anterograde amnesia refers to the inability to recall events or facts introduced since the amnesia began.

The diagnostic manual used by clinicians, called the Diagnostic and Statistical Manual of Mental Disorders (DSM), lists three classifications of amnestic disorders , described below.

Amnestic disorder due to a general medical condition

The memory loss of amnestic disorder due to a general medical condition can be transient or chronic. This disorder can manifest as retrograde or anterograde loss. For diagnosis, the person must experience impairment of social or occupational functioning that differs from their normal levels, and the memory loss cannot occur as part of dementia or delirium. The medical condition responsible must be confirmed by patient history or by physical exam or lab results.

Substance-induced persisting amnestic disorder

Substance-induced persisting amnestic disorder can occur with use of alcohol, sedatives, hypnotics, or anxiolytics. Methotrexate, a chemotherapy drug, can induce it, as can some toxins, including lead, mercury, carbon monoxide, insecticides, or industrial solvents. There are subtypes, including alcohol-induced persisting amnestic disorder. In the alcohol-induced form, the symptoms of Wernicke-Korsakoff syndrome may manifest as a result of the thiamine deficiency. Full recovery is not the norm with alcohol-induced amnestic disorder but is possible when caused by other drugs. The diagnostic criteria for the substance-induced form of amnestic disorder are similar to those for that induced by a general medical condition, except that the history should show exposure to the substance involved.

Amnestic disorder not otherwise specified

If the characteristics of the amnesia do not fit either of the above categories, the disorder is then classified as amnestic disorder not otherwise specified, generally because the causative agent/event is not known.

Dissociative amnesia

Dissociative amnesia is part of a different group of disorders, the dissociative disorders. It manifests as an inability to remember information that is personally important, but possibly traumatic or stressful. It was previously called Psychogenic amnesia. The memory impairment in this disorder is reversible, and memory loss can be of several types. It can be localized, in which the missing memory covers a defined period of time, or it can be selective, so that only bits and pieces of a situation are recalled. There are also three less common types: generalized (memories covering a lifetime are missing); continuous (memories are missing from a specific time period up to the present); and systematized (only memories from specific categories of information are missing, such as the names of family members). This disorder can arise in a person of any age.

Amnesia is not always obvious to the casual observer—motor skills such as tying shoelaces and bike riding are retained, as is the ability to read and comprehend the meaning of words. Because of this phenomenon, researchers have suggested that there is more than one area of the brain used to store memory. General knowledge and perceptual skills may be stored in a memory separate from the one used to store personal facts.

Childhood amnesia, a term coined by Anna Freud in the late 1940s, refers to the fact that most people cannot recall childhood experiences during the first three to five years of life. It has been suggested that this type of amnesia occurs because children and adults organize memories in different ways. The differences are based on the brain’s physical development and communication among the different areas of the brain involved in developing memory. Others believe children begin remembering facts and events once they have accumulated enough experience to be able to relate experiences to each other.

See alsoAmnestic disorders; Dissociative amnesia; Dissociative fugue.

Resources

BOOKS

American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, 4th ed., Text rev. Washington, D.C.: American Psychiatric Association, 2000.

OTHER

Martin, Peter R., Charles, K. Singleton, and Susanne Hiller-Sturmhoefel. National Institute of Alcohol Abuse and Alcoholism. “The Role of Thiamine Deficiency in Alcoholic Brain Disease.” <http://pubs.niaaa.nih.gov/publications/arh27-2/134-142.htm> (2006).

National Institute on Alcohol Abuse and Alcoholism. “Alcohol’s Damaging Effects on the Brain.” <http://pubs.niaaa.nih.gov/publications/aa63/aa63.htm>.

National Institute of Neurological Disorders and Stroke. “Wernicke-Korsakoff Syndrome Information Page.” <http://www.ninds.nih.gov/disorders/wernicke_korsakoff/wernicke-korsakoff.htm>.

Emily Jane Willingham, PhD