Amnesia classification
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2]; Associate Editor(s)-in-Chief: Aditya Govindavarjhulla, M.B.B.S. [3]; Jesus Rosario Hernandez, M.D. [4]
Overview
Amnesia can classified based upon various neuropsychopathologies. It is important to consider the etiological, organic, progressive and clinical criteria in amnesia classification. Amnesia can be classified based on the temporal nature of the amnesia, which is anterograde if the person forgets what occurs after the inciting event, or retrograde if the person forgets everything that occured before the inciting event. Amnesia can also be classified based upon the nature, type, and pathophysiology of the amnestic episode.
Classification
Temporal Classification of Amnesia
Anterograde Amnesia
Anterograde amnesia is a form of amnesia, or memory loss, in which new events are not transferred from short-term memory to long-term memory. This may be a permanent deficit, or it may be temporary, such as is sometimes seen for a period of hours or days after head trauma or for a period of intoxication with an amnestic drug. The deficit makes its sufferers unable to recall an event which occurred only moments earlier when their attention has shifted to something else. Those who have theoretically pure anterograde amnesia are still able to access memories formed before its onset, but they exist in a transient world where anything beyond their immediate attention span disappears from their consciousness permanently. However, theoretically pure anterograde amnesia rarely surfaces: in reality, long-term cases nearly always occur with some degree of retrograde amnesia.
Anterograde amnesia is often informally, but incorrectly, called "short-term memory loss", conjuring up the idea, as in the movie Memento, that it is a problem of short-term memory. For this reason, formal (correct technical or scientific) usage demands the term anterograde amnesia, since the deficit is not in short-term memory, but rather in encoding into more permanent, long-term memory.
"Traveler's amnesia" is a temporary form of anterograde amnesia in which victims may, for instance, realize they have changed planes during a memory gap or discover that they rented a car. This condition is caused by some medications, notably imidazopyridines and benzodiazepines, especially when they are used as sleep aids. Although medical researchers characterize this side effect as "less common", the benzodiazepine triazolam (Halcion) apparently has the greatest chance of inducing traveler's amnesia, whether taken exactly as directed, varying the dosage (say, when coming off the drug too quickly), drinking alcohol, or not getting enough sleep. However, benzodiazepines alprazolam (Xanax) and nitrazepam (Mogadon) are also more likely to be at fault, the former on its own and the latter when the victim is sleep-deprived or in some way changing the dose.
Criminals may use medications with anterograde amnesic effects for date rape. Unbeknownst to the victim, the perpetrator uses drugs such as flunitrazepam, temazepam, and other common substances, usually in a drink, to cause disorientation; incapacitation; unconsciousness; distortions in vision, time, sense, and identity; and an uninhibited state, the hallmark of which is anterograde amnesia.
Amnesia automatism is usually induced by prescription drugs, frequently but not necessarily in association with moderate alcohol intake. Victims have memory gaps for a period shortly after taking the drug concerned, which causes embarrassment and fear for what might have happened. Dis-inhibited and uncharacteristic behavior (sometimes together with carrying out quite complex tasks - e.g. cooking and serving a nice meal, but in the nude) is sometimes witnessed during such episodes, which adds further embarrassment and distress.
Retrograde Amnesia
Retrograde amnesia is a form of amnesia where someone will be unable to recall events that occurred before the onset of amnesia. The term is used to categorize patterns of symptoms, rather than to indicate a particular cause or etiology. Both retrograde amnesia and anterograde amnesia can occur together in the same patient, and commonly result from damage to the brain regions most closely associated with episodic/declarative memory: the medial temporal lobes and especially the hippocampus.
Retrograde amnesia is caused by trauma that results in brain injury. Critical details of the physical changes in the brain that cause retrograde amnesia are still unknown. Retrograde amnesia is often temporally graded, meaning that remote memories are more easily accessible than events occurring just prior to the trauma (Ribot's Law). Events nearest in time to the accident that caused memory loss may never be recovered.
The memory loss may just affect specific “classes” of memory. For instance the victim, a concert pianist before, may still remember what a piano is after the onset of retrograde amnesia, but may forget how to play. The relearning rate for often used skills such as typing and math is typically faster than if they had never learned it before. While there is no cure for retrograde amnesia, “jogging” the victim’s memory by exposing them to significant articles from their past will speed the rate of recall.
The victim of retrograde amnesia may feel embarrassed or stressed that they no longer remember key people and significant events. Typically the victim may be overwhelmed by the rush of well-wishers who seek to reacquaint themselves. It is important to let the amnesiac go at his or her “own pace,” so they are not overly stressed. Forgotten relations forget that they are effectively meeting the victim for the “first time” and may make the victim uncomfortable through displays of friendship such as kissing or slapping on the back that, while appropriate for longtime relationships, are not appropriate for “first time” meetings.
These terms are used to categorize patterns of symptoms, rather than to indicate a particular cause or etiology. Both categories of amnesia can occur together in the same patient, and commonly result from drug effects or damage to brain regions most closely associated with episodic/declarative memory: the medial temporal lobes and 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) and an inability to recall the hospital ward where he is told he had conversations with family over the past two days (anterograde amnesia).
Other Types of Amnesia
Dissociative or Functional or Psychogenic Amnesia
Psychogenic amnesia, also known as functional or dissociative amnesia, is a disorder characterized by abnormal memory functioning in the absence of structural brain damage or a known neurobiological cause; severe cases are very rare.[1] It is defined by the presence of retrograde amnesia or the inability to retrieve stored memories and events leading up to the onset of amnesia and an absence of anterograde amnesia or the inability to form new long term memories.[2][3][4] In most cases, patients lose their autobiographical memory and personal identity even though they are able to learn new information and perform everyday functions normally. Other times, there may be a loss of basic semantic knowledge and procedural skills such as reading and writing.[5]
There are two types of psychogenic amnesia, global and situation-specific.[5][6] Global amnesia, also known as fugue state, refers to a sudden loss of personal identity that lasts a few hours to days.[4] This is preceded by severe stress and/or depressed mood. Fugue state is very rare, and usually resolves over time, often helped by therapy.[7] Situation-specific amnesia is a type of dissociative amnesia occurs as a result of a severely stressful event, as in post-traumatic stress disorder. Dissociative amnesia is due to psychological rather than physiological causes and can sometimes be helped by therapy.[7]
Dissociative Amnesia can include :
Repressed Memory
Repressed memory is one of the most controversial subjects in the history of psychology and psychiatry. A repressed memory, according to some theories of psychology, is a memory (often traumatic) of an event or environment which is stored by the unconscious mind but outside the awareness of the conscious mind. Some theorize that these memories may be recovered (that is, integrated into consciousness) years or decades after the event, often via therapy. They may also reoccur in dreams. The theory of dissociative amnesia makes the assumption that memory repression is possible. Conservative estimates show that at least ten percent of all people sexually abused in childhood will experience periods of total amnesia for the abuse they suffered. This will be followed by delayed recall experiences.[8] Peer reviewed and clinical studies continue to document the existence of recovered memory. [9] There are over one hundred corroborated cases of recovered memory in legal, clinical and scientific case studies.[10] The repressed memory concept was popularized during the 1980s and partly the 1990s by the popular press, some feminist groups, and some psychological schools of thought; however it is suffering a retreat in popularity with professionals and the public during recent years after a series of scandals, lawsuits, and license revocations concerning it.[11] The concept was originated by Sigmund Freud in his 1896 essay Zur Ätiologie der Hysterie ("On the etiology of hysteria"), however Freud himself abandoned his theory between 1897-1905, and during 1920-1923 replaced it with his impulse-based concept of Id, Super-ego, and Ego. Friedrich Nietzsche was the first to suggest an active, conscious thought management method in the second essay of his On the Genealogy of Morals as a necessary fundamental of efficiency, responsibility, and maturity. The theory of repressed memories must not be confused with the established psychological concept of repression in general which stresses impulses instead of memories. This contrasts with anterograde amnesia caused by amnestics such as benzodiazepines or alcohol, where an experience was prevented from being transferred from temporary to permanent memory storage because it was never stored in the first place.
Dissociative Fugue
A Fugue state is a state of mind characterized by abandonment of personal identity, along with the memories, personality and other identifying characteristics of individuality. The Fugue state is a condition of Dissociative Fugue (formerly Psychogenic Fugue) (DSM-IV Dissociative Disorders 300.13[12]).
The etiology of the fugue state is related to Dissociative Amnesia, (DSM-IV Codes 300.12[13]) which has several other subtypes: selective amnesia, generalized amnesia, continuous amnesia, systematized amnesia, in addition to the subtype dissociative fugue[12].
Unlike retrograde amnesia (which is popularly referred to simply as "amnesia", the state where someone completely forgets who they are), dissociative amnesia is not due to the direct physiological effects of a substance (e.g., a drug of abuse, a medication, DSM-IV Codes 291.1 & 292.83) or a neurological or other general medical condition (e.g., Amnestic Disorder due to a head trauma, DSM-IV Codes 294.0).[14] It is a complex neuropsychological process.[15]
As the person experiencing a Dissociative fugue may have recently suffered the reappearance of an event or person representing an earlier life trauma, the emergence of an armoring or defensive personality seems to be for some, a logical apprehension of the situation. Therefore, the terminology fugue state may carry a slight linguistic distinction from dissociative fugue, the former implying a greater degree of motion. For the purposes of this article then, a fugue state would occur while one is acting out a dissociative fugue.
- Sudden, unexpected travel away from home or one's customary place of work, with inability to recall one's past
- Confusion about personal identity, or the assumption of a new identity
- Significant distress or impairment.
The Merck Manual[16] defines dissociative fugue 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.
In support of this definition, the Merck Manual [16] further defines dissociative amnesia as:
- An inability to recall important personal information, usually of a traumatic or stressful nature, that is too extensive to be explained by normal forgetfulness.
Posthypnotic Amnesia
Posthypnotic amnesia is where events during hypnosis are forgotten, or where past memories are unable to be recalled.
Lacunar Amnesia
Lacunar amnesia is the loss of memory about one specific event. It is a type of amnesia that leaves a lacuna (a gap) in the record of memory.
Childhood Amnesia
Childhood amnesia is the common inability of adults to remember the earliest years of their childhood. Infantile, or childhood amnesia is characterized by the relative absence of memory before 3 or 4 years of age. It is important to note that the term does not refer to complete absence of memories, but the relative scarcity of memories during infancy — a scarcity that cannot be accounted for by a forgetting curve. Additionally, the boundary is malleable and can be influenced by both individual experiences (Usher & Neisser, 1993) and cultural factors (Wang, 2001). Research has demonstrated that children are adept learners and are quick to acquire and retain information. Children do remember events; however, these memories accessible as children are lost to infantile amnesia in adulthood (Bauer, 2004; Fivush, et al., 1987). Whilst Sigmund Freud attributed this to sexual repression, others have theorized that this may be due to language development or immature parts of the brain.
Post-traumatic Amnesia
Post-traumatic amnesia (PTA) is a state of confusion that occurs immediately following a traumatic brain injury in which the injured person is disoriented and unable to remember events that occur after the injury.[17] The person may be unable to state his or her name, where he or she is, and what time it is.[17] When continuous memory returns, PTA is considered to have resolved.[18] While PTA lasts, new events cannot be stored in the memory.[19] About a third of patients with mild head injury are reported to have "islands of memory", in which the patient can recall only some events.[19] Both retrograde and anterograde forms may be referred to as PTA,[20] or the term may be used to refer only to anterograde amnesia.[21]
Frequently the last symptom to ameliorate after a loss of consciousness,[20] anterograde amnesia may not develop until hours after the injury.[22] A common example in sports concussion is the quarterback who was able to conduct the complicated mental tasks of leading a football team after a concussion, but has no recollection the next day of the part of the game that took place after the injury. Retrograde amnesia sufferers may partially regain memory later, but memories are not regained with anterograde amnesia because they were not encoded properly.[23]
Transient Global Amnesia
Transient global amnesia (TGA), is an anxiety-producing temporary loss of short-term memory. TGA presents as anterograde amnesia, with unawareness of the surroundings and multiple questions regarding the surroundings. Retrograde amnesia may also be present sometimes. Typically, patients are not be able to remember events from the past few hours, and are not able to retain new information for more than a few minutes. Patients with transient global amnesia suffer the effects of TGA for 1 to 10 hours, the mean duration of amnesia being 6 hours. After an episode of TGA the symptoms resolve completely, before 24 hours. The cognitive functioning of the patient otherwise is normal.[24]
Global amnesia is a total loss of the memory. It is an extremely rare form of amnesia, and can occur as a result of diverse etiologies.[25]
Source Amnesia
The disorder is particularly episodic, where source or contextual information surrounding facts are severely distorted or unable to be recalled. Via the use of the Wisconsin Card Sorting Task (WCST) developed by Esta Berg in 1948, Positron Emission Tomography (PET), and explicit and implicit memory tests, researchers have performed extensive empirical research on source-amnesiacs and concluded or suggested neuropsychological genesis.
Daniel Schacter and Endel Tulving have each proposed that memory for facts is differentiated from memory for context. The neuropsychological implications as in brain maturation, deterioration in the normal aging course, and damage are conveyed. The organic deterioration of the frontal lobes in the process of normal aging has a greater influence on episodic memory than perhaps premature lobes in young children. Source amnesia has the ability to alter one's confidence in their memory encoded in differing conditions (i.e. conscious state or in dreaming), as in memory distrust syndrome, an inclusive disorder. Source amnesia was first presented and examined in the hypnotic environment, and further understanding the human memory process is essential in unraveling this condition.
As source amnesia prohibits recollection of the context specific information surrounding facts in experienced events, there is also the inclusive case of confusion concerning the content or context of events, a highly attributable factor to confabulation in brain disease. Such confusion was termed memory distrust syndrome by Gudjonsson and MacKeith.
A condition similar to source amnesia sometimes occurs in dreams, when the dreamer has some knowledge about details of the imaginary environment but has no idea how they learned this information.
Memory Distrust Syndrome
As source amnesia prohibits recollection of the context-specific information surrounding facts in experienced events, there is also the inclusive case of confusion concerning the content or context of events, a highly attributable factor to confabulation in brain disease. Such confusion has been loosely termed memory distrust syndrome by Gudjonsson and MacKeith in 1982. A person who suffers from memory distrust syndrome may distrust his or her own memory and be motivated to rely on external (non-self) sources.
The overwhelming propensity to accept information from external sources (i.e. an interrogator) based on the influence of susceptibility has led to well documented false confessions. In addition, the credibility of a witness account who suffers from memory distrust syndrome is more questionable. In a parallel situation, amnesic individuals may have a greater propensity to have their memory manipulated and perhaps perform non-advantageous acts on the "direction" of external sources and have difficulty in differentiating imaginary and real experiences. Since it is an identified and natural occurrence that source amnesia pathology exists in the criminal law system, psychiatrists should increasingly take assessment and identification measures to isolate such a disorder on accused individuals and eye-witnesses.
Blackout Phenomenon
A blackout is a phenomenon caused by the intake of alcohol in which long term memory creation is impaired. Blackouts are frequently described as having effects similar to that of anterograde amnesia. 'Blacking out' is not to be confused with the mutually exclusive act of 'passing out'. Blackouts can generally be divided into two categories, "en bloc" blackouts, and "fragmentary" blackouts. En bloc blackouts are classified by the inability to later recall any memories from the intoxicated period, even when prompted. These blackouts are characterized also by the ability to easily recall things that have occurred within the last 2 minutes, yet inability to recall anything prior to this period. As such, a person experiencing an en bloc blackout may not appear to be doing so, as they can carry on conversations or even manage to accomplish difficult feats such as driving cars. It is difficult to determine the end of this type of blackout as sleep typically occurs before they end.[26] Fragmentary blackouts are characterized by the ability to recall certain events from an intoxicated period, yet be unaware that other memories are missing until reminded of the existence of these 'gaps' in memory. Research indicates that fragmentary blackouts are far more common than en bloc blackouts.[27]
Korsakoff's Syndrome
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.
References
- ↑ Brandt J, Van Gorp WG (2006). "Functional ("psychogenic") amnesia". Semin Neurol. 26 (3): 331–40. doi:10.1055/s-2006-945519. PMID 16791779.
- ↑ Markowitsch HJ (2003). "Psychogenic amnesia". Neuroimage. 20 Suppl 1: S132–8. PMID 14597306.
- ↑ Yasuno F, Nishikawa T, Nakagawa Y; et al. (2000). "Functional anatomical study of psychogenic amnesia". Psychiatry Res. 99 (1): 43–57. PMID 10891648.
- ↑ 4.0 4.1 Mackenzie Ross S (2000). "Profound retrograde amnesia following mild head injury: organic or functional?". Cortex. 36 (4): 521–37. PMID 11059453.
- ↑ 5.0 5.1 Serra L, Fadda L, Buccione I, Caltagirone C, Carlesimo GA (2007). "Psychogenic and organic amnesia: a multidimensional assessment of clinical, neuroradiological, neuropsychological and psychopathological features". Behav Neurol. 18 (1): 53–64. PMID 17297220.
- ↑ Kopelman MD (2002). "Disorders of memory". Brain. 125 (Pt 10): 2152–90. PMID 12244076. Retrieved 2008-04-05.
- ↑ 7.0 7.1 Myers, Catherine E. (2006). "Memory Loss & The Brain". Rutgers University. Retrieved 2007-12-05.
- ↑ Recovered Memories of Sexual Abuse Scientific Research & Scholarly Resources by Jim Hopper, PhD.
- ↑ Recovered Memory Project
- ↑ Recovered Memory Project Archive
- ↑ Robbins Susan P.,The Social and Cultural Context of Satanic Ritual Abuse Allegations, published in Institute for Psychological Therapies magazine, vol 10 1998.[1]
- ↑ 12.0 12.1 12.2 Dissociative Fugue (formerly Psychogenic Fugue) ( DSM-IV 300.13, Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition)
- ↑ Dissociative Amnesia, DSM-IV Codes 300.12 ( Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition )
- ↑ Complete List of DSM-IV Codes ( PsychNet-UK.com )
- ↑ Background to Dissociation ( The Pottergate Centre for Dissociation & Trauma )
- ↑ 16.0 16.1 Merck Manual 1999 section 15 (Psychiatric Disorders), chapter 188 (Dissociative Disorders)
- ↑ 17.0 17.1 Lee LK (2007). "Controversies in the Sequelae of Pediatric Mild Traumatic Brain Injury". Pediatric Emergency Care. 23 (8): 580–583, quiz 584–586. doi:10.1097/PEC.0b013e31813444ea. PMID 17726422.
- ↑ Petchprapai N, Winkelman C (2007). "Mild Traumatic Brain Injury: Determinants and Subsequent Quality of Life. A Review of the Literature". Journal of Neuroscience Nursing. 39 (5): 260–272. PMID 17966292.
- ↑ 19.0 19.1 van der Naalt J (2001). "Prediction of Outcome in Mild to Moderate Head Injury: A Review". Journal of Clinical and Experimental Neuropsychology. 23 (6): 837–851. doi:10.1076/jcen.23.6.837.1018. PMID 11910548.
- ↑ 20.0 20.1 Cantu RC (2001). "Posttraumatic Retrograde and Anterograde Amnesia: Pathophysiology and Implications in Grading and Safe Return to Play". Journal of Athletic Training. 36 (3): 244–248. PMID 12937491.
- ↑ Sivák Š, Kurča E, Jančovič D, Petriščák Š, Kučera P (2005). "An Outline of the Current Concepts of Mild Brain Injury with Emphasis on the Adult Population" (PDF). Časopis Lėkařů Českých. 144 (7): 445–450.
- ↑ Binder LM (1986). "Persisting Symptoms after Mild Head Injury: A Review of the Postconcussive Syndrome". Journal of Clinical and Experimental Neuropsychology. 8 (4): 323–346. doi:10.1080/01688638608401325. PMID 3091631.
- ↑ Rees PM (2003). "Contemporary Issues in Mild Traumatic Brain Injury". Archives of Physical Medicine and Rehabilitation. 84 (12): 1885–1894. PMID 14669199.
- ↑ Bartsch T, Alfke K, Stingele R, Rohr A, Freitag-Wolf S, Jansen O; et al. (2006). "Selective affection of hippocampal CA-1 neurons in patients with transient global amnesia without long-term sequelae". Brain. 129 (Pt 11): 2874–84. doi:10.1093/brain/awl248. PMID 17003071.
- ↑ Quinette P, Guillery-Girard B, Dayan J, de la Sayette V, Marquis S, Viader F; et al. (2006). "What does transient global amnesia really mean? Review of the literature and thorough study of 142 cases". Brain. 129 (Pt 7): 1640–58. doi:10.1093/brain/awl105. PMID 16670178.
- ↑ GOODWIN, D.W; CRANE, J.B.; AND GUZE, S.B. Alcoholic "blackouts": A review and clinical study of 100 alcoholics. American Journal of Psychiatry 126:191-198, 1969.
- ↑ WHITE, A.M.; SIGNER, M.L.; KRAUS, C.L.; AND SWARTZWELDER, H.S. Experiential aspects of alcohol-induced blackouts among college students. American Journal of Drug and Alcohol Abuse, 2004 in press.