This article needs more reliable medical references for verification or relies too heavily on primary sources. Please review the contents of the article and add the appropriate references if you can. Unsourced or poorly sourced material may be challenged and removed. Find sources: "Amnesia" – news · newspapers · books · scholar · JSTOR (March 2019)

Other namesAmnesic syndrome
SpecialtyPsychiatry, neurology

Amnesia is a deficit in memory caused by brain damage or brain diseases,[1] but it can also be temporarily caused by the use of various sedative and hypnotic drugs. The memory can be either wholly or partially lost due to the extent of damage that is caused.[2]

There are two main types of amnesia:

These two types are not mutually exclusive; both can also occur simultaneously.[4]

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 have shown a correlation between deficiency of RbAp48 protein and memory loss. Scientists were able to find that mice with damaged memory have a lower level of RbAp48 protein compared to normal, healthy mice.[5][6] In people with amnesia, the ability to recall immediate information is still retained,[7][8][9] 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. People can learn new procedural knowledge. In addition, priming (both perceptual and conceptual) can assist amnesiacs in the learning of fresh non-declarative knowledge.[1] Individuals with amnesia also retain substantial intellectual, linguistic, and social skills despite profound impairments in the ability to recall specific information encountered in prior learning episodes.[10][11][12]

The term is from Ancient Greek 'forgetfulness'; from ἀ- (a-) 'without', and μνήσις (mnesis) 'memory'.

Signs and symptoms

Individuals with amnesia can learn new information, particularly if the information is non-declarative knowledge. However, in some situations, people with dense anterograde amnesia do not remember the episodes during which they previously learned or observed the information. Some people with amnesia show abnormal amount of memory loss, confusion, and difficulty recalling other people or places. People who recover often do not remember having amnesia.[13]

Declarative information

Declarative memory can be broken down into semantic memory and episodic memory. Semantic memory being that of facts, episodic memory being that of memory related to events.

While a patient with amnesia might have a loss of declarative memory, this loss might vary in severity as well as the declarative information that it affects, depending on many factors. For example, LSJ was a patient who had retrograde declarative memory loss as the result of bilateral medial temporal lobe damage, but she was still able to remember how to perform some declarative skills. She was able to remember how to read music and the techniques used in art. She had preserved skill-related declarative memory for some things even though she had deficits in other declarative memory tasks. She even scored higher on skill-related declarative memory than the control in watercolor techniques, a technique that she used in her professional career before she acquired amnesia.[14]

Semantic information

The loss of semantic information in amnesia is most closely related with damage to the medial temporal lobe[15] or to the neocortex.[16]

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. There is evidence that the hippocampus and the medial temporal lobe may help to consolidate semantic memories, but then they are more correlated with the neocortex. While lesions of the hippocampus normally lead to the loss of episodic memory, if there is any effect on semantic memory, it is more varied and usually does not last as long.[16]

Episodic information

One reason that patients could not form new episodic memories is likely because the CA1 region of the hippocampus has a lesion, and thus the hippocampus could not make connections to the cortex. After an ischemic episode (an interruption of the blood flow to the brain), an MRI of patient R.B. following surgery showed his hippocampus to be intact except for a specific lesion restricted to the CA1 pyramidal cells.[1][17] In one instance, transient global amnesia was caused by a hippocampal CA1 lesion. While this was a temporary case of amnesia, it still shows the importance of the CA1 region of the hippocampus in memory.[18] Episodic memory loss is most likely to occur when there has been damage to the hippocampus. There is evidence that damage to the medial temporal lobe correlates to a loss of autobiographical episodic memory.[16]

Non-declarative information

Some retrograde and anterograde amnesiacs are capable of non-declarative memory, including implicit learning and procedural learning. For example, some patients show improvement on the pseudorandom sequences experiment just as healthy people; therefore, procedural learning can proceed independently of the brain system required for declarative memory. Some patients with amnesia are able to remember skills that they had learned without being able to consciously recall where they had learned that information. For example, they may learn to do a task and then be able to perform the task later without any recollection of learning the task.[19] 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 declarative 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 demonstrated by some patients, such as K.C. and H.M, who have medial temporal damage and anterograde amnesia, still have perceptual priming. Priming was accomplished in many different experiments of amnesia, and it was found that the patients can be primed; they have no conscious recall of the event, but the response is there.[20] Those patients did well in the word fragment completion task.[1][better source needed] There is some evidence that non-declarative memory can be held onto in the form of motor skills. This idea was disputed, though, because it is argued that motor skills require both declarative and non-declarative information.[14]


There are three generalized categories in which amnesia could be acquired by a person.[21] 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 subcategory of the first.

Among specific causes of amnesia are the following:




Many forms of amnesia fix themselves without being treated.[50] However, there are a few ways to cope with memory loss if treatment is needed. Since there are a variety of causes that form different amnesia, there are different methods that response better with the certain type of amnesia. Emotional support and love as well as medication and psychological therapy have been proven effective.[13]

One technique for amnesia treatment 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.[51] This may also include strategies for organizing information to remember it more easily and for improving understanding of lengthy conversation.[52]

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.[51] Notebooks, wall calendars, pill reminders and photographs of people and places are low-tech memory aids that can help as well.[52]

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.[53][unreliable medical source?] 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 treat it.[54][55] Treating alcoholism and preventing alcohol and illicit drug use can prevent further damage, but in most cases will not recover lost memory.[52]

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.[56]


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.[57]

Case studies have 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 several extremely important case studies: Henry Molaison, R.B, and G.D.

Henry Molaison

Henry Molaison, formerly known as H.M., changed the way people thought of memory. The case was first reported in a paper by William Beecher Scoville and Brenda Milner in 1957.[58] He was a patient who had severe epilepsy attributed to a bicycle accident at the age of nine. Physicians were unable to control his seizures with drugs, so the neurosurgeon Scoville tried a new approach involving brain surgery. He 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 had even been given a list in the first place.[59] However, H.M.'s working and short-term memory seemed to be intact. He had a normal digit span and could hold a conversation that did not require him to recall past parts of the conversation.[60] Once Molaison stopped thinking about the lists he was unable to recall them again from long-term memory. This gave researchers evidence that short-term and long-term memory are in fact two different processes.[61] Even though he forgot about the lists, he was still 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.[62] In some studies it was found that H.M.'s perceptual learning was intact and that his other cognitive skills were working appropriately. It was also found that some people with declarative information amnesia are able to be primed.[60]

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 had happened since his surgery. However, he could still remember things that had 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.[59] After his death Molaison donated his brain to science, where they were able to discover the areas of the brain that had the lesions which caused his amnesia, particularly the medial temporal lobe.[61] This case study provided important insight to the areas of the brain that are affected in anterograde amnesia, as well as how amnesia works. H.M.'s case showed that memory processes are consolidated into different parts of the brain and that short-term and working memory are not usually impaired in cases of amnesia.[60]

Clive Wearing

Another famous historical case of amnesia was that of Clive Wearing. Clive Wearing was a conductor and musician who contracted herpes simplex virus. This virus affected the hippocampal regions of the brain. Because of this damage, Wearing was unable to remember information for more than a few moments.[63] Wearing's non-declarative memory was still functioning but his declarative memory was impaired. To him, he felt that he had just come to consciousness for the first time every time he was unable to hold on to information. This case also can be used as evidence that there are different memory systems for declarative and non-declarative memory. This case was more evidence that the hippocampus is an important part of the brain in remembering past events and that declarative and non-declarative memories have different processes in different parts of the brain.

Patient R.B.

Patient R.B. was a normally functioning man until the age of 52. At age 50, he had been diagnosed with angina and had surgery for heart problems on two occasions. 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, with the exception of a couple of years before his surgery, and presented no sign of any other cognitive impairment. It was not 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.[64]

Patient G.D.

Patient G.D. was a white male born in 1940 who served in the Navy. He was diagnosed with chronic kidney failure and received hemodialysis treatment for the rest of his life. In 1983, he went to the hospital for elective parathyroidectomy. He also had a left thyroid lobectomy because of severe loss of blood in his left lobe. He began having cardiac problems as a result of the surgery and became very agitated. Even five days after being released from the hospital he was unable to remember what had happened to him. Aside from memory impairment, none of his other cognitive processes seemed to be affected. He did not want to be involved in much research, but through memory tests he took with doctors, they were able to ascertain that his memory problems were present for the next 9.5 years until his death. After he died, his brain was donated to science, photographed, and preserved for future study.[65]

In fiction

Global amnesia is a common motif in fiction despite being extraordinarily rare in reality. In the introduction to his anthology The Vintage Book of Amnesia, Jonathan Lethem writes:

Real, diagnosable amnesia – people getting knocked on the head and forgetting their names – is mostly just a rumor in the world. It's a rare condition, and usually a brief one. In books and movies, though, versions of amnesia lurk everywhere, from episodes of Mission Impossible to metafictional and absurdist masterpieces, with dozens of stops in between. Amnesiacs might not much exist, but amnesiac characters stumble everywhere through comic books, movies, and our dreams. We've all met them and been them.[66]

Lethem traces the roots of literary amnesia to Franz Kafka and Samuel Beckett, among others, fueled in large part by the seeping into popular culture of the work of Sigmund Freud, which also strongly influenced genre films such as film noir. Amnesia is so often used as a plot device in films, that a widely recognized stereotypical dialogue has even developed around it, with the victim melodramatically asking "Where am I? Who am I? What am I?", or sometimes inquiring of their own name, "Bill? Who's Bill?"[66]

In movies and television, particularly sitcoms and soap operas, it is often depicted that a second blow to the head, similar to the first one which caused the amnesia, will then cure it. In reality, however, repeat concussions may cause cumulative deficits including cognitive problems, and in extremely rare cases may even cause deadly swelling of the brain associated with second-impact syndrome.[67]

In science fiction involving a masquerade that hides magical or alien societies from humanity, such as Men in Black or the SCP Foundation, fictional organizations can induce deliberate amnesia via drugs or advanced technology to wipe the minds of those that view supernatural phenomena.

See also


  1. ^ a b c d e 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. ^ David X. Cifu; Henry L. Lew (10 September 2013). Handbook of Polytrauma Care and Rehabilitation. Demos Medical Publishing. ISBN 978-1-61705-100-5.
  5. ^ Pavlopoulos, Elias; Jones, Sidonie; Kosmidis, Stylianos; Close, Maggie; Kim, Carla; Kovalerchik, Olga; Small, Scott A.; Kandel, Eric R. (28 August 2013). "Molecular mechanism for age-related memory loss: the histone-binding protein RbAp48". Science Translational Medicine. 5 (200): 200ra115. doi:10.1126/scitranslmed.3006373. ISSN 1946-6242. PMC 4940031. PMID 23986399.
  6. ^ Kosmidis, Stylianos; Polyzos, Alexandros; Harvey, Lucas; Youssef, Mary; Denny, Christine A.; Dranovsky, Alex; Kandel, Eric R. (23 October 2018). "RbAp48 Protein Is a Critical Component of GPR158/OCN Signaling and Ameliorates Age-Related Memory Loss". Cell Reports. 25 (4): 959–973.e6. doi:10.1016/j.celrep.2018.09.077. ISSN 2211-1247. PMC 7725275. PMID 30355501.
  7. ^ Dewar, Michaela; Della Sala, Sergio; Beschin, Nicoletta; Cowan, Nelson (2010). "Profound retroactive interference in anterograde amnesia: What interferes?". Neuropsychology. 24 (3): 357–367. doi:10.1037/a0018207. ISSN 1931-1559. PMC 2864945. PMID 20438213.
  8. ^ Baddeley, Alan; Wilson, Barbara A. (April 2002). "Prose recall and amnesia: implications for the structure of working memory". Neuropsychologia. 40 (10): 1737–1743. doi:10.1016/S0028-3932(01)00146-4. PMID 11992661. S2CID 22404837 – via Elsevier Science Direct.
  9. ^ Benson, D. Frank (1978). "Amnesia". Southern Medical Journal. 71 (10): 1221–1227. doi:10.1097/00007611-197810000-00011. PMID 360401. S2CID 220554752.
  10. ^ LS., Cermak (1984). The episodic-semantic distinction in amnesia. New York: Guilford Press. p. 55.
  11. ^ M, Kinsbourne (1975). Short-term memory processes and the amnesiac syndrome. New York: Academic. pp. 258–91.
  12. ^ H, Weingartner (1983). Forms of cognitive failure. Sc alzheimerience. pp. 221:380–2.
  13. ^ a b Services, Department of Health & Human. "Amnesia". Retrieved 3 December 2019.
  14. ^ a b c Gregory, Emma; McCloskey, Michael; Ovans, Zoe; Landau, Barbara (18 May 2016). "Declarative memory and skill-related knowledge: Evidence from a case study of amnesia and implications for theories of memory". Cognitive Neuropsychology. 33 (3–4): 220–240. doi:10.1080/02643294.2016.1172478. ISSN 0264-3294. PMID 27315433. S2CID 39581659.
  15. ^ Buckner, Randy L. (November 2000). "Neural origins of 'I remember'". Nature Neuroscience. 3 (11): 1068–1069. doi:10.1038/80569. ISSN 1097-6256. PMID 11036258. S2CID 29593573.
  16. ^ a b c Rosenbaum, R. Shayna; Moscovitch, Morris; Foster, Jonathan K.; Schnyer, David M.; Gao, Fuqiang; Kovacevic, Natasha; Verfaellie, Mieke; Black, Sandra E.; Levine, Brian (August 2008). "Patterns of Autobiographical Memory Loss in Medial-Temporal Lobe Amnesic Patients". Journal of Cognitive Neuroscience. 20 (8): 1490–1506. doi:10.1162/jocn.2008.20105. ISSN 0898-929X. PMID 18303977. S2CID 1097954.
  17. ^ Bartsch, Thorsten; Döhring, Juliane; Rohr, Axel; Jansen, Olav; Deuschl, Günther (18 October 2011). "CA1 neurons in the human hippocampus are critical for autobiographical memory, mental time travel, and autonoetic consciousness". Proceedings of the National Academy of Sciences. 108 (42): 17562–17567. Bibcode:2011PNAS..10817562B. doi:10.1073/pnas.1110266108. ISSN 0027-8424. PMC 3198338. PMID 21987814.
  18. ^ Yokota, Hiroshi; Yokoyama, Kazuhiro; Iwasaki, Satoru (2015). "Transient global amnesia with intracranial vertebral artery dissection and hippocampal CA1 lesion". Neurology India. 63 (4): 604–5. doi:10.4103/0028-3886.162077. ISSN 0028-3886. PMID 26238898.
  19. ^ Butters, N; Delis, D C; Lucas, J A (January 1995). "Clinical Assessment of Memory Disorders in Amnesia and Dementia". Annual Review of Psychology. 46 (1): 493–523. doi:10.1146/ ISSN 0066-4308. PMID 7872736.
  20. ^ Hamann, Stephan B.; Squire, Larry R. (November 1997). "Intact Priming for Novel Perceptual Representations in Amnesia". Journal of Cognitive Neuroscience. 9 (6): 699–713. doi:10.1162/jocn.1997.9.6.699. ISSN 0898-929X. PMID 23964593. S2CID 13097336.
  21. ^ Services, Department of Health & Human. "Amnesia".
  22. ^ Myers, David G. Psychology. fifth ed. New York: Worth Publishers, 1998. N. pag. Print
  23. ^ Benbow, SM (2004) "Adverse effects of ECT". In AIF Scott (ed.) The ECT Handbook, second edition. Archived 21 April 2012 at the Wayback Machine London: The Royal College of Psychiatrists, pp. 170–174.
  24. ^ 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. doi:10.1176/ajp.126.2.191. PMID 5804804.
  25. ^ Parker ES; Birnbaum IM; Noble EP (December 1976). "Alcohol and memory: Storage and state dependency". Journal of Verbal Learning and Verbal Behavior. 15 (6): 691–702. doi:10.1016/0022-5371(76)90061-X.
  26. ^ Carlson, N. R. (19992000). Memory. Psychology: the science of behaviour (Canandian ed., p. 250). Scarborough, Ontario: Allyn and Bacon Canada.
  27. ^ Buckley, Mark J. (July 2005). "The Role of the Perirhinal Cortex and Hippocampus in Learning, Memory, and Perception". The Quarterly Journal of Experimental Psychology Section B. 58 (3–4b): 246–268. doi:10.1080/02724990444000186. ISSN 0272-4995. PMID 16194968. S2CID 21091079.
  28. ^ a b Erdogan, Serap (2010). "Anterograde Amnesia" (PDF). Psikiyatride Guncel Yaklasimlar-Current Approaches in Psychiatry. 2 (2): 174–189. Retrieved 27 November 2011.
  29. ^ Van Der Hart, Onno; Nijenhuis, Ellert (October 2001). "Generalized Dissociative Amnesia: Episodic, Semantic and Procedural Memories lost and found". Australian & New Zealand Journal of Psychiatry. 35 (5): 589–600. doi:10.1080/0004867010060506. ISSN 0004-8674. PMID 11551273. S2CID 1443531.
  30. ^ Barash, Jed A.; Ganetsky, Michael; Boyle, Katherine; Raman, Vinod; Toce, Michael S.; Kaplan, Scott; Lev, Michael H.; Worth, Jonathan L.; DeMaria, Alfred (2018). "Acute Amnestic Syndrome Associated with Fentanyl Overdose". New England Journal of Medicine. 378 (12): 1157–1158. doi:10.1056/NEJMc1716355. ISSN 1533-4406. PMID 29562161.
  31. ^ Mastin, L. (2010). The human memory: Retrograde amnesia. Retrieved from
  32. ^ "memory abnormality." Encyclopædia Britannica. Encyclopædia Britannica Online Academic Edition. Encyclopædia Britannica Inc., 2012. Web. 21 April 2012.
  33. ^ Kirwan et al., 2008
  34. ^ Masferrer, Roberto; Masferrer, Mauricio; Prendergast, Virginia; Harrington, Timothy R (2000). "Grading Scale for Cerebral Concussions". BNI Quarterly. 16 (1). ISSN 0894-5799. Retrieved 5 February 2017.
  35. ^ Bourget Dominique, Whitehurst Laurie (2007). "Amnesia and crime". Journal of the American Academy of Psychiatry and the Law Online. 35 (4): 469–480. PMID 18086739.
  36. ^ Loewenstein, Richard J. (1996). Handbook of dissociation. Boston, MA: Springer. pp. 307–336. doi:10.1007/978-1-4899-0310-5_15.
  37. ^ "Dissociative Fugue. Retrieved 7 August 2012". Archived from the original on 4 November 2012. Retrieved 22 December 2012.
  38. ^ Coons, Philip M. (1 September 2016). "Psychogenic or Dissociative Fugue: A Clinical Investigation of Five Cases". Psychological Reports. 84 (3): 881–886. doi:10.2466/pr0.1999.84.3.881. PMID 10408212. S2CID 39673692.
  39. ^ Carlson, Neil (2007). Psychology the Science of Behaviour. Toronto: Pearson. p. 283. ISBN 978-0-205-64524-4. OCLC 441151384.
  40. ^ Enea Violeta, Dafinoiu Ion (2008). "Posthypnotic amnesia and autobiographical memory in adolescents". Journal of Evidence-Based Psychotherapies. 8 (2): 201.
  41. ^ Wang, Qi (January 2003). "Infantile amnesia reconsidered: A cross-cultural analysis". Memory. 11 (1): 65–80. doi:10.1080/741938173. ISSN 0965-8211. PMID 12653489. S2CID 40591244.
  42. ^ Hayne, Harlene; Jack, Fiona (2011). "Childhood amnesia". Wiley Interdisciplinary Reviews: Cognitive Science. 2 (2): 136–145. doi:10.1002/wcs.107. PMID 26302005.
  43. ^ Schacter, D.L.; Harbluk, J.L.; McLachlen, D.R. (1984). "Retrieval without recollection: an experimental analysis of source amnesia". Journal of Verbal Learning and Verbal Behavior. 23 (5): 593–611. doi:10.1016/s0022-5371(84)90373-6.
  44. ^ Johnson, M K (29 November 1997). "Source monitoring and memory distortion". Philosophical Transactions of the Royal Society B: Biological Sciences. 352 (1362): 1733–1745. doi:10.1098/rstb.1997.0156. ISSN 0962-8436. PMC 1692093. PMID 9415926.
  45. ^ a b Spiegel, David R (June 2011). "A Case of Probable Korsakoff's Syndrome: A Syndrome of Frontal Lobe and Diencephalic Structural Pathogenesis and a Comparison with Medial Temporal Lobe Dementias". Innovations in Clinical Neuroscience. 8 (6): 15–19. PMC 3140893. PMID 21779537.
  46. ^ Arts, Nicolaas JM; Walvoort, Serge JW; Kessels, Roy PC (27 November 2017). "Korsakoff's syndrome: a critical review". Neuropsychiatric Disease and Treatment. 13: 2875–2890. doi:10.2147/NDT.S130078. ISSN 1176-6328. PMC 5708199. PMID 29225466.
  47. ^ Walsh RD, Jr; Wharen RE, IV; Tatum WO (2011). "Complex transient epileptic amnesia". Epilepsy & Behavior. 20 (2): 410–413. doi:10.1016/j.yebeh.2010.12.026. PMID 21262589. S2CID 32333979.
  48. ^ Murray, B. D.; Kensinger, E. A. (2012). "Semantic Memory in Profound Amnesia". Encyclopedia of the Sciences of Learning. Boston, MA: Springer. pp. 3022–3025.
  49. ^ "Semantic Variant Primary Progressive Aphasia". Memory and Aging Center. Retrieved 3 December 2019.
  50. ^ "Amnesia: Management and Treatment". Cleveland Clinic. 29 July 2020. Archived from the original on 29 November 2020. Retrieved 22 August 2020.
  51. ^ a b "Treating Amnesia". Neurology Now. 4 (4): 37. 2008. doi:10.1097/01.NNN.0000333846.54546.f8.
  52. ^ a b c "Amnesia - Symptoms and causes". Mayo Clinic. Retrieved 6 January 2024.
  53. ^ Mandal, A. (n.d) Treatment of Amnesia. News Medical. Retrieved From:
  54. ^ "Thiamin". Linus Pauling Institute. 12 October 2021. Retrieved 6 January 2024.
  55. ^ Akhouri, Shweta; Kuhn, James; Newton, Edward J. (2023), "Wernicke-Korsakoff Syndrome", StatPearls, Treasure Island (FL): StatPearls Publishing, PMID 28613480, retrieved 6 January 2024
  56. ^ Benson DF (October 1978). "Amnesia". Southern Medical Journal. 71 (10): 1221–1227. doi:10.1097/00007611-197810000-00011. ISSN 0038-4348. PMID 360401. S2CID 220554752.
  57. ^ Ribot, T. (1882). Diseases of Memory: An essay in the positive psychology. London: D. Appleton and company.
  58. ^ Scoville, W.B.; Milner, B. (1957). "Loss of recent memory after bilateral hippocampal lesions". Journal of Neurology, Neurosurgery, and Psychiatry. 20 (1): 11–21. doi:10.1136/jnnp.20.1.11. PMC 497229. PMID 13406589.
  59. ^ a b Corkin, S.; Milner, B.; Teuber, H. (1968). "Further Analysis of the Hippocampal Amnesic Syndrome: 14-Year Follow-up Study on Patient H.M." (PDF). Neuropsychologia. 6 (3): 215–234. doi:10.1016/0028-3932(68)90021-3.
  60. ^ a b c Eichenbaum, Howard (January 2013). "What H.M. taught us". Journal of Cognitive Neuroscience. 25 (1): 14–21. doi:10.1162/jocn_a_00285. ISSN 1530-8898. PMID 22905817. S2CID 7900357.
  61. ^ a b Draaisma, D. (2013). "Neuroscience: Losing the past". Nature. 497 (7449): 313–314. Bibcode:2013Natur.497..313D. doi:10.1038/497313a.
  62. ^ Rosenbaum, R. S.; Murphy, K. J.; Rich, J. B. (2012). "The amnesias". Wiley Interdisciplinary Reviews: Cognitive Science. 3 (1): 47–63. doi:10.1002/wcs.155. PMID 26302472.
  63. ^ Kopelman, Michael; Morton, John (28 January 2005), "Psychogenic Amnesias: Functional Memory Loss", Recovered Memories: Seeking the Middle Ground, John Wiley & Sons, Ltd, pp. 219–243, doi:10.1002/0470013486.ch11, ISBN 978-0-470-01348-9
  64. ^ Zola-Morgan, S; Squire, LR; Amaral, DG (1986). "Human amnesia and the medial temporal region: Enduring memory impairment following a bilateral lesion limited to field CA1 of the hippocampus". The Journal of Neuroscience. 6 (10): 2950–2967. doi:10.1523/JNEUROSCI.06-10-02950.1986. PMC 6568782. PMID 3760943.
  65. ^ Rempel-Clower, NL; Zola, SM; Squire, LR; Amaral, DG (1996). "Three cases of enduring memory impairment after bilateral damage limited to the hippocampal formation". The Journal of Neuroscience. 16 (16): 5233–5255. doi:10.1523/JNEUROSCI.16-16-05233.1996. PMC 6579309. PMID 8756452.
  66. ^ a b Lethem, Jonathan (ed.) The Vintage Book of Amnesia New York: Vintage, 2000 ISBN 0-375-70661-5
  67. ^ "Special Report: Cumulative Concussions". BrainLine. 6 May 2014. Retrieved 8 October 2020.