For other uses, see Amnesia (disambiguation).
"Amnesiac" redirects here. For the Radiohead album, see Amnesiac (album).
| Amnesia |
| Classification and external resources |
| ICD-10 |
F04, R41.3 |
| ICD-9 |
294.0, 780.9, 780.93 |
| MedlinePlus |
003257 |
| MeSH |
D000647 |
Amnesia (from Greek Ἀμνησία) is a deficit in memory caused by brain damage, disease, or psychological trauma. [1] Essentially, amnesia is the loss of memory. The memory can be either wholly or partially lost due to the extent of damage that was caused.[2] There are two main types of amnesia: anterograde amnesia and retrograde amnesia. Anterograde amnesia is the inability to form new long term memories, and retrograde amnesia is when previously formed memories are lost. In some cases, the memory loss extends back decades, whereas in other cases the person only losses a few months of memory. Anterograde and retrograde amnesia are not mutually exclusive. Both can occur within a patient at one time.
Case studies show that amnesia is typically associated with damage to the medial temporal lobe. In addition, specific areas of the hippocampus (The CA1 region) are involved with memory. Research has also shown that amnesia also can occur when areas of the diencephalon are damaged. People suffering with amnesia may still be able to form new memories. Studies have shown that patients can learn new procedural knowledge. In addition, priming (both perceptual and conceptual) can assist amnesiacs in the learning of new non-declarative knowledge. [1]
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Contents
- 1 Discovery of amnesia
- 1.1 Important case studies
- 1.1.1 Henry Molaison
- 1.1.2 Patient R.B.
- 2 Causes of amnesia
- 3 Types of amnesia
- 4 Acquisition of new memories
- 4.1 Acquisition of new declarative information
- 4.2 Acquisition of new non-declarative information
- 5 Treatment
- 6 See also
- 7 References
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Discovery of amnesia
French psychologist Theodule-Armand Ribot was among the first scientists to study amnesia. He proposed Ribot’s Law which states that there is a time gradient in retrograde amnesia. The law follows a logical progression of memory loss due to disease. First, a patient loses the recent memories, then personal memories, and finally intellectual memories. He implied that the most recent memories were lost first. [3]
Important case studies
Case studies played a large role in the discovery of amnesia and the parts of the brain that were affected. The studies gave important insight into how amnesia affects the brain. There are two extremely important case studies: Henry Molaison and R.B.
Henry Molaison
Henry Molaison, formerly known as H.M., was a patient who suffered from severe epilepsy. Physicians were unable to control his seizures with drugs, so they tried a new approach involving brain surgery. Doctors removed his medial temporal lobe bilaterally by doing a temporal lobectomy. His epilepsy did improve, but Molaison lost the ability to form new long-term memories (anterograde amnesia). He exhibited normal short-term memory ability. Studies were completed consistently throughout Molaison’s lifetime to discover more about amnesia.[1] Researchers did a 14 year follow up study on Molaison. They studied him for a period of two weeks to learn more about his amnesia. After 14 years, Molaison still could not recall things that have happened since his surgery. However, he can still remember things that happened prior to the operation. Researchers also found that, when asked, Molaison could answer questions about national or international events, but he could not remember his own personal memories.[4] This case study provided important insight to the areas of the brain that were affected in anterograde amnesia, as well as how amnesia works.
Patient R.B.
After an ischemic episode (reduction of blood to the brain) that was caused from a heart bypass surgery, R.B. lost his memory. Unlike Molaison, R.B. developed both anterograde and retrograde amnesia. His lesions were restricted to the hippocampus. It wasn’t until after his death, that researcher’s had the chance to examine his brain. They found that his lesions were restricted to the CA1 portion of the hippocampus. This case study led to important research involving the role of the hippocampus and the function of memory. [5]
Causes of amnesia
There are three generalized categories in which amnesia could be acquired by a person. The three categories are head trauma (example: head injuries), traumatic events (example: seeing something devastating to the mind), or physical deficiencies (example: atrophy of the hippocampus). The majority of amnesia and related memory issues derive from the first two categories as these are more common and the third could be considered a sub category of the first.
- Head trauma is a very broad range as it deals with any kind of injury or active action toward the brain which might cause amnesia. Retrograde and Anterograde amnesia are more often seen from events like this, an exact example of a cause of the two would be electroshock therapy, which would cause both briefly for the receiving patient.
- Traumatic events are more subjective as, what is traumatic is dependent on what the person finds to be traumatic. Regardless a traumatic event is an event where something so distressing occurs that the mind chooses to forget rather than deal with the stress. A common example of amnesia that is caused by traumatic events is dissociative amnesia, which occurs when the person forgets an event that has deeply disturbed them.[6] An example would be forgetting what happened to your friends after you see them harmed in a gruesome fashion.
- Physical deficiencies are different from head trauma as physical lean more toward passive physical issues. The difference would be having surgery that removes part of your brain, this would be active and thus head trauma, while the surgery caused the surrounding areas to atrophy, which is passive. Henry Molaison is a great example of physical deficiencies as parts of his brain began to atrophy after his surgery.[1]
Amongst specific causes of amnesia are the following:
- Electroconvulsive therapy in which seizures are electrically induced in patients for therapeutic effect can have acute effects including both retrograde and anterograde amnesia.[7]
- Alcohol can both cause blackouts[8] and have deleterious effects on memory formation.[9]
Types of amnesia
- Anterograde amnesia refers to the inability to create new memories due to brain damage. The brain damage can be caused by the effects of long-term alcoholism, severe malnutrition, stroke, head trauma, surgery, Wernicke-Korsakoff Syndrome, cerebrovascular events, anoxia or other trauma.[10] The two brain regions related with this condition are medial temporal lobe and medial diencephalon. Anterograde amnesia can't be treated with pharmacological methods due to neuronal loss.[11] However, treatment exists in educating patients to define their daily routines and after several steps they begin to benefit from their procedural memory. Likewise, social and emotional support is critical to improving quality of life for anterograde amnesia sufferers.[11]
- Retrograde amnesia refers to inability to recall memories before onset of amnesia. One may be able to encode new memories after the incident. Retrograde is usually caused by head trauma or brain damage to parts of the brain besides the hippocampus. The hippocampus is responsible for encoding new memory. Episodic memory is more likely to be affected that semantic memory. The damage is usually caused by head trauma, cerebrovascular accident, stroke, tumor, hypoxia, encephalitis, or chronic alcoholism. People suffering from retrograde amnesia are more likely to remember general knowledge rather than specifics. Recent memories are less likely to be recovered but older memories will be easier to recall due to strengthening over time.[12] Retrograde amnesia is usually temporary and can be treated by exposing them to memories from the loss.[13]
- Post-traumatic amnesia is generally due to a head injury (example: a fall, a knock on the head). Traumatic amnesia is often transient, but may be permanent 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. Having longer periods of amnesia or consciousness after an injury may be an indication that recovery from remaining concussion symptoms will take much longer.[14]
- 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 disaster. The memory is stored in long term memory, but access to it is impaired because of psychological defense mechanisms. Persons retain the capacity to learn new information and there may be some later partial or complete recovery of memory. 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. An individual with dissociative fugue disorder is unaware or confuse about their identity and will travel in journeys away from their surrounding to discover or create new identities.[15] The Merck Manual defines it as " one or more episodes of amnesia in which patients cannot recall some or all of their past and either lose their identity or form a new identity. The episodes, called fugues, result from trauma or stress. Dissociative fugue often manifests as sudden, unexpected, purposeful travel away from home."[16] While popular in fiction, it is extremely rare.
- Post-hypnotic amnesia is where events during hypnosis are forgotten, or where past memories are unable to be recalled. The failure to remember those events are induced by suggestions made during the hypnosis.[17]
- 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. Researchers have found that implicit memories cannot be recalled and are hardily described. Remembering how to play the piano are common examples of implicit memory. Explicit memories, on the other hand, can be recalled and described in words. Remembering the first day that you met your piano teacher is an example of explicit memories.[18]
- Transient global amnesia is a well-described medical and clinical phenomenon. This form of amnesia is distinct in that abnormalities in the hippocampus can sometimes be visualized using a special form of magnetic resonance imaging of the brain known as diffusion-weighted imaging (DWI). Symptoms typically last for less than a day and there is often no clear precipitating factor or any other neurological deficits. The cause of this syndrome is not clear. The hypothesis of the syndrome includes transient reduced blood flow, possible seizure or an atypical type of migraine. Patients are typically amnestic of events more than a few minutes in the past, though immediate recall is usually preserved.
- Source amnesia is the inability to remember where, when or how previously learned information has been acquired, while retaining the factual knowledge.[19] Source amnesia is both part of ordinary forgetting and can be a memory disorder caused by different factors.[20] People suffering from source amnesia can also get confused about the content of what is remembered. This confusion has been loosely termed memory distrust syndrome. Individuals who suffer from this syndrome distrusts their memory and may be motivated to rely on external (non-self) sources.[20]
- 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. It should be noted that the person's short term memory may appear to be normal, however the person may have a difficult time attempting to recall a past story, or with unrelated words, as well as complicated patterns.[21]
- 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.
- Prosopamnesia is the inability to recognize or 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.
Acquisition of new memories
Patients with amnesia can learn new information, particularly non-declarative knowledge. However, some patients with dense anterograde amnesia do not remember the episodes during which they learn or observe the information previously.
Acquisition of new declarative information
Some patients with anterograde amnesia can still acquire some semantic information, even though it might be more difficult and might remain rather unrelated to more general knowledge. H.M. could accurately draw a floor plan of the home in which he lived after surgery, even though he had not lived there in years. The reason why those patients couldn’t form new episodic memories could be that the CA1 region of the hippocampus was lesioned, and thus the hippocampus couldn’t make connections to the cortex. After an ischemic episode following surgery, an MRI of patient R.B. showed his hippocampus to be intact except for a specific lesion restricted to the CA1 pyramidal cells. [1]
Acquisition of new non-declarative information
Some retrograde and anterograde amnesics are capable of nondeclarative memory, including implicit learning and procedural learning. For example, some patients show improvement on the pseudorandom sequences experiment as healthy people do. Therefore, procedural learning can proceed independently of the brain system required for episodic memory. According to fMRI studies, the acquisition of procedural memories activates the basal ganglia, the premotor cortex and the supplementary motor area, regions which are not normally associated with the formation of episodic memories.
This type of dissociation between declarative and procedural memory can also be found in patients with diencephalic amnesia such as Korsakoff’s syndrome.
Another example is that some patients, such as K.C. and H.M, who have medial temporal damage and anterograde amnesia still have perceptual priming. Those patients did well in the word fragment completion test. [1]
Treatment
Many forms of amnesia fix themselves without being treated.[22] However, there are a few ways to cope with memory loss if that is not the case. One of these ways is cognitive or occupational therapy. In therapy, amnesiacs will develop the memory skills they have and try to regain some they have lost by finding which techniques help retrieve memories or create new retrieval paths.[23] This may also include strategies for organizing information to remember it more easily and for improving understanding of lengthy conversation.[24]
Another coping mechanism is taking advantage of technological assistance. A personal digital to keep track of day-to-day tasks. Reminders can be set up for appointments, when to take medications, birthdays and other important events. Many pictures can also be stored to help amnesiacs remember names of friends, family and co-workers.[23] Notebooks, wall calendars, pill reminders and photographs of people and places are low-tech memory aids that can help as well.[24]
While there are no medications available to treat amnesia, underlying medical conditions can be treated to improve memory. Such conditions include but are not limited to low thyroid function, liver or kidney disease, stroke, depression, bipolar disorder and blood clots in the brain.[25] Wernicke—Korsakoff syndrome involves a lack of thiamin and replacing this vitamin by consuming thiamin-rich foods such as whole grain cereals, legumes (beans and lentils), nuts, lean pork, and yeast can help.[22] Treating alcoholism and preventing alcohol and illicit drug use can prevent further damage but in most cases will not recover lost memory.[24]
See also
- Betrayal trauma
- Doug Bruce
- Emotion and memory
- False memory
- KC (patient)
- Benjaman Kyle
- List of films featuring mental illness
- Memory erasure
- Repressed memories
- Mr. Nobody
- Transient epileptic amnesia
- Clive Wearing
References
- ^ a b c d e f Gazzaniga, M., Ivry, R., & Mangun, G. (2009) Cognitive Neuroscience: The biology of the mind. New York: W.W. Norton & Company.
- ^ "Amnesia." The Gale Encyclopedia of Science. Ed. K. Lee Lerner and Brenda Wilmoth Lerner. 4th ed. Vol. 1. Detroit: Gale, 2008. 182-184. Gale Virtual Reference Library.
- ^ Ribot, T. (1882) Diseases of Memory: An essay in the positive psychology. London: D. Appleton and company.
- ^ Corkin, S., Milner,B. & Teuber, H. (1968) Further Analysis of the Hippocampal Amnesic Syndrome: 14-Year Follow-up Study on Patient H.M. Neuropsychologia. 6, 215-234.
- ^ Burgess, N., Maguire, E., Spiers, H. (2001) Hippocampal Amnesia. Neurocase. 7, 357-382.
- ^ Myers, David G. Psychology. fifth ed. New York: Worth Publishers, 1998. N. pag. Print
- ^ Benbow, SM (2004) "Adverse effects of ECT". In AIF Scott (ed.) The ECT Handbook, second edition. London: The Royal College of Psychiatrists, pp. 170–174.
- ^ Goodwin DW, Crane JB, Guze SB (August 1969). "Alcoholic "blackouts": a review and clinical study of 100 alcoholics". Am J Psychiatry 126 (2): 191–8. PMID 5804804. http://ajp.psychiatryonline.org/article.aspx?volume=126&page=191.
- ^ Parker ES, Birnbaum IM, Noble EP (December 1976). "Alcohol and memory: Storage and state dependency". Journal of Verbal Learning and Verbal Behaviour 15 (6): 691–702. doi:10.1016/0022-5371(76)90061-X. http://www.sciencedirect.com/science/article/pii/002253717690061X.
- ^ Carlson, N. R. (19992000). Memory. Psychology: the science of behaviour (Canandian ed., p. 250). Scarborough, Ont.: Allyn and Bacon Canada.
- ^ a b Erdogan, Serap (2010). "Anterograde Amnesia". Psikiyatride Guncel Yaklasimlar-Current Approaches In Psychiatry 2 (2): 174–189. http://www.cappsy.org/archives/vol2/no2/cap_02_10.pdf. Retrieved 27 November 2011.
- ^ Mastin, L. (2010). The human memory: Retrograde amnesia . Retrieved from http://www.human-memory.net/disorders_retrograde.html
- ^ "memory abnormality." Encyclopædia Britannica. Encyclopædia Britannica Online Academic Edition. Encyclopædia Britannica Inc., 2012. Web. 21 Apr 2012.
- ^ Masferrer R, Masferrer M, Prendergast V, Harrington TR (2000). "Grading Scale for Cerebral Concussions" ([dead link]). BNI Quarterly (Barrow Neurological Institute) 16 (1). ISSN 0894-5799
- ^ http://my.clevelandclinic.org/disorders/dissociative_disorders/hic_dissociative_fugue.aspx Dissociative Fugue. Retrieved 7 August 2012
- ^ The Merck Manuals Online
- ^ Carlson, Neil (2007). Psychology the Science of Behaviour. Toronto: Pearson. p. 283. ISBN 978-0-205-64524-4.
- ^ Harlene Hayne*, Fiona Jack, [1], Wiley Interdisciplinary Reviews: Cognitive Science, March/April 2011
- ^ Schacter, D.L., Harbluk, J.L., and McLachlen, D.R. (1984). Retrieval without recollection: an experimental analysis of source amnesia. Journal of Verbal Learning and Verbal Behaviour, 23(5): 593-611.
- ^ a b Shaheen Emmanuel Lakhan: Neuropsychological Generation of Source Amnesia: An Episodic Memory Disorder of the Frontal Brain. Journal of Medicine, Volume 1, Issue 1, 2007
- ^ "Types of Amnesia". uwaterloo. http://ahsmail.uwaterloo.ca/kin356/amnesia/amnesia2.html. Retrieved 9 April 2012.
- ^ a b Nordquist, C. (2004) What is Amnesia? What Causes Amnesia? Medical News Today. Retrieved from: http://www.medicalnewstoday.com/articles/9673.php
- ^ a b Treating Amnesia. Neurology Now. 4(4), pg. 37 (2008)
- ^ a b c Mayo Clinic Staff (2011) Amnesia: Treatments and Drugs. Mayo Clinic. Retrieved from: http://www.mayoclinic.com/health/amnesia/DS01041/DSECTION=treatments-and-drugs.
- ^ Mandal, A. (n.d) Treatment of Amnesia. News Medical. Retrieved From: http://www.news-medical.net/health/Treatment-of-amnesia.aspx
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proc(eval/thrp), drug(N5A/5B/5C/6A/6B/6D)
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