Amnesia

From Wikipedia, the free encyclopedia - View original article

Amnesia
Classification and external resources
ICD-10F04, R41.3
ICD-9294.0, 780.9, 780.93
MedlinePlus003257
MeSHD000647
 
  (Redirected from Amnesiac)
Jump to: navigation, search
Amnesia
Classification and external resources
ICD-10F04, R41.3
ICD-9294.0, 780.9, 780.93
MedlinePlus003257
MeSHD000647

Amnesia (from Greek ἀμνησία, "ἀ" meaning "without", "μνησία" memory) is a deficit in memory caused by brain damage, disease, or psychological trauma.[1] Amnesia can also be caused temporarily by the use of various sedatives and hypnotic drugs. Essentially, amnesia is 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: retrograde amnesia and anterograde amnesia. Retrograde amnesia is the inability to retrieve information that was acquired before a particular date, usually the date of an accident or operation.[3] In some cases the memory loss can extend back decades, while in others the person may lose only a few months of memory. Anterograde amnesia is the inability to transfer new information from the short-term store into the long-term store. People with this type of amnesia cannot remember things for long periods of time. These two types are not mutually exclusive. Both can occur within a patient at one time. Case studies, such as that of patient R.B., show that both types of amnesia can occur simultaneously. Case studies also show that amnesia is typically associated with damage to the medial temporal lobe. In addition, specific areas of the hippocampus (the CA1 region) are involved with memory. Research has also shown that when areas of the diencephalon are damaged, amnesia can occur. Recent studies has showed the correlation between the Deficiency of RbAp48 protein and Memory Loss. Scientists were able to find that mice, with damaged memory, have a lower level of RbAp48 protein compare to normal, healthy mice.

In people suffering with amnesia the ability to recall immediate information is still retained,[4][full citation needed] and they may still be able to form new memories. However, a severe reduction in the ability to learn new material and retrieve old information can be observed. Patients can learn new procedural knowledge. In addition, priming (both perceptual and conceptual) can assist amnesiacs in the learning of fresh non-declarative knowledge.[1] Amnesic patients also retain substantial intellectual, linguistic, and social skill despite profound impairments in the ability to recall specific information encountered in prior learning episodes.[5][6][7]

Discovery[edit]

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.[8]

Important case studies[edit]

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. The studies also gave scientists the resources into improving their knowledge about amnesia and insight into a cure or prevention. There are two extremely important case studies: Henry Molaison and R.B.

Henry Molaison[edit]

Henry Molaison, formerly known as H.M., changed the way people thought of memory. He 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. If he was given a list of words, he would forget them in about a minute's time. In fact, he would forget that he was even given a list in the first place. He was able to learn things through his implicit memory. The psychologists would ask him to draw something on a piece of paper, but to look at the paper using a mirror. Though he could never remember ever doing that task, he would improve after doing it over and over again. This showed the psychologists that he was learning and remembering things unconsciously.[9] 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.[10] This case study provided important insight to the areas of the brain that are affected in anterograde amnesia, as well as how amnesia works.

Patient R.B.[edit]

After an ischemic episode (reduction of blood to the brain) that was caused from a heart bypass surgery, R.B. demonstrated a loss of anterograde memory, but almost no loss of retrograde memory and presented no sign of any other cognitive impairment. It wasn’t until after his death that researchers had the chance to examine his brain, when they found his lesions were restricted to the CA1 portion of the hippocampus. This case study led to important research involving the role of the hippocampus and the function of memory.[11]

Causes[edit]

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.

Amongst specific causes of amnesia are the following:

Types[edit]

Acquisition of new memories[edit]

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 learned or observed the information previously.

Acquisition of new declarative information[edit]

Some patients with anterograde amnesia can still acquire some semantic information, even though it might be more difficult and might remain rather unrelated to more general knowledge. H.M. could accurately draw a floor plan of the home in which he lived after surgery, even though he had not lived there in years. The reason patients couldn’t form new episodic memories is likely because 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[edit]

Some retrograde and anterograde amnesics are capable of non-declarative memory, including implicit learning and procedural learning. For example, some patients show improvement on the pseudorandom sequences experiment as healthy people do. Therefore, procedural learning can proceed independently of the brain system required for 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[edit]

Many forms of amnesia fix themselves without being treated.[29] 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.[30] This may also include strategies for organizing information to remember it more easily and for improving understanding of lengthy conversation.[31]

Another coping mechanism is taking advantage of technological assistance, such as a personal digital device to keep track of day-to-day tasks. Reminders can be set up for appointments, when to take medications, birthdays and other important events. Many pictures can also be stored to help amnesiacs remember names of friends, family and co-workers.[30] Notebooks, wall calendars, pill reminders and photographs of people and places are low-tech memory aids that can help as well.[31]
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.[32] 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.[29] Treating alcoholism and preventing alcohol and illicit drug use can prevent further damage, but in most cases will not recover lost memory.[31]

Although improvements occur when patients receive certain treatments, there is still no actual cure remedy for amnesia so far. To what extent the patient recovers and how long the amnesia will continue depends on the type and severity of the lesion.[33]

See also[edit]

References[edit]

  1. ^ 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.
  2. ^ "Amnesia." The Gale Encyclopedia of Science. Ed. K. Lee Lerner and Brenda Wilmoth Lerner. 4th ed. Vol. 1. Detroit: Gale, 2008. 182-184. Gale Virtual Reference Library.
  3. ^ Schacter, Daniel. L "Psychology"
  4. ^ D. Frank Benson, "AMNESIA"
  5. ^ LS., Cermak (1984). The episodic-semantic distinction in amnesia. New York: Guilford Press. p. 55. 
  6. ^ M, Kinsbourne (1975). Short-term memory processes and the amnesic syndrome. New York: Academic. pp. 258–91. 
  7. ^ H, Weingartner (1983). Forms of cognitive failure. Science. pp. 221:380–2. 
  8. ^ Ribot, T. (1882) Diseases of Memory: An essay in the positive psychology. London: D. Appleton and company.
  9. ^ http://onlinelibrary.wiley.com.myaccess.library.utoronto.ca/doi/10.1002/wcs.155/full
  10. ^ 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.
  11. ^ Zola-Morgan, S., Squire, L.R. & Amaral,D.G. (1986). Human amnesia and the medial temporal region: enduring memory impairment following a bilateral lesion limited to field CA1 of the hippocampus. Journal of Neuroscience, 6, 2950-2967.
  12. ^ Myers, David G. Psychology. fifth ed. New York: Worth Publishers, 1998. N. pag. Print
  13. ^ 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.
  14. ^ 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. 
  15. ^ 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. 
  16. ^ Carlson, N. R. (19992000). Memory. Psychology: the science of behaviour (Canandian ed., p. 250). Scarborough, Ont.: Allyn and Bacon Canada.
  17. ^ a b Erdogan, Serap (2010). "Anterograde Amnesia". Psikiyatride Guncel Yaklasimlar-Current Approaches in Psychiatry 2 (2): 174–189. Retrieved 27 November 2011. 
  18. ^ Mastin, L. (2010). The human memory: Retrograde amnesia . Retrieved from http://www.human-memory.net/disorders_retrograde.html
  19. ^ "memory abnormality." Encyclopædia Britannica. Encyclopædia Britannica Online Academic Edition. Encyclopædia Britannica Inc., 2012. Web. 21 Apr 2012.
  20. ^ 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
  21. ^ "Dissociative Fugue. Retrieved 7 August 2012". My.clevelandclinic.org. Retrieved 2012-12-22. 
  22. ^ "The Merck Manuals Online". Merckmanuals.com. Retrieved 2012-12-22. 
  23. ^ Carlson, Neil (2007). Psychology the Science of Behaviour. Toronto: Pearson. p. 283. ISBN 978-0-205-64524-4. OCLC 441151384. 
  24. ^ Harlene Hayne*, Fiona Jack, [1], Wiley Interdisciplinary Reviews: Cognitive Science, March/April 2011
  25. ^ 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.
  26. ^ 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". Scientificjournals.org. Retrieved 2012-12-22. 
  27. ^ "Types of Amnesia". uwaterloo. Retrieved 9 April 2012. 
  28. ^ Walsh RD, Jr Wharen RE, IV Tatum WO (2011). "Complex transient epileptic amnesia". Epilepsy & Behaviour 20 (2): 410–413. doi:10.1016/j.yebeh.2010.12.026. 
  29. ^ a b Nordquist, C. (2004) What is Amnesia? What Causes Amnesia? Medical News Today. Retrieved from: http://www.medicalnewstoday.com/articles/9673.php
  30. ^ a b "Treating Amnesia. Neurology Now. 4(4), pg. 37 (2008)". Journals.lww.com. doi:10.1097/01.NNN.0000333846.54546.f8. Retrieved 2012-12-22. 
  31. ^ 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.
  32. ^ Mandal, A. (n.d) Treatment of Amnesia. News Medical. Retrieved From: http://www.news-medical.net/health/Treatment-of-amnesia.aspx
  33. ^ Benson, DF (October 1978). "Amnesia". Southern Medical Journal 71 (10): 1221 – 1227. doi:10.1097/00007611-197810000-00011. ISSN 0038-4348. PMID 360401.