Retrograde amnesia

In neurology, retrograde amnesia (RA) is the inability to access memories or information from before an injury or disease occurred.[1] RA differs from a similar condition called anterograde amnesia (AA), which is the inability to form new memories following injury or disease onset.[2] Although an individual can have both RA and AA at the same time, RA can also occur on its own; this 'pure' form of RA can be further divided into three types: focal, isolated, and pure RA.[3] RA negatively affects an individual's episodic, autobiographical, and declarative memory, but they can still form new memories because RA leaves procedural memory intact.[3] Depending on its severity, RA can result in either temporally graded or more permanent memory loss.[3] However, memory loss usually follows Ribot's law, which states that individuals are more likely to lose recent memories than older memories.[4] Diagnosing RA generally requires using an Autobiographical Memory Interview (AMI) or observing brain structure through magnetic resonance imaging (MRI), a computed tomography scan (CT), or electroencephalography (EEG).[3][5]


Types of RA can be divided into two main categories: temporally graded RA and pure forms of RA. Individuals with pure forms of RA like focal, isolated, and pure RA do not have anterograde amnesia (AA).
Types of RA can be divided into two main categories: temporally graded RA and pure forms of RA. Individuals with pure forms of RA like focal, isolated, and pure RA do not have anterograde amnesia (AA).

Temporally graded

Memory loss in patients with temporally graded RA strongly follows Ribot's law, meaning that one will experience more memory loss for events closer to the injury or disease onset.[4] This type of RA is commonly triggered in individuals with Korsakoff syndrome due to a combination of effects from long-term alcohol use and Wernicke encephalopathy.[6] Debate has risen about why this temporal gradient forms in the first place. Initial theories proposed that the hippocampus and medial temporal lobe are not nearly as important for long-term memories compared to short-term memories.[3] As memory processing occurs in the brain, neocortical regions can directly communicate with each other over time and thus do not rely as heavily on the hippocampus for long-term memory storage.[3] Hence, if an individual experiences retrograde amnesia that damages the hippocampus, they will lose less long-term memories compared to short-term memories. This theory has been challenged by the multiple-trace theory, which claims that the brain develops a hippocampal trace each time a memory is retrieved.[3] Since more hippocampal traces are present for older memories, it is easier for older memories to remain intact when RA occurs.[3]

Focal, isolated, and pure

An absence of anterograde amnesia (AA) characterizes pure forms of RA, which fall into three main categories: focal, isolated, and pure RA.[3] Slight differences in the use of these terms to describe a pure form of RA are summarized below:

Pure Forms of RA
Focal RA Isolated RA Pure RA
Focal RA generally results from neurological problems like epilepsy and is characterized by memory loss prior to – but not after – injury or disease onset.[7] When an individual experiences focal RA, a combination of their episodic and semantic memories may be affected.[8] Take a case study of a middle-aged female, for instance, who experienced focal RA after significant head trauma.[8] Although she could be re-taught information from her past, these memories were not episodic, but rather, semantic.[8] With focal RA, the details of a patient's life prior to amnesia onset can be reintroduced, but they are unable to recall how they perceived the experience.[8] Isolated RA is usually associated with a visible thalamic lesion.[9] Consistent with other forms of RA, the isolated form is marked by the inability to recall past information.[9] Take the case a middle-aged man coined JG, whose thalamic lesion expanded as he grew older.[9] This lesion growth induced his isolated RA, resulting in both autobiographical memory loss and the inability to recognize information from popular culture.[9] Pure RA (PRA) is caused by a range of factors such as vascular diseases, encephalitis, and head injuries.[10] It is often confused with peritraumatic amnesia that may follow mild concussions, but the severity and duration of PRA differs from that of peritraumatic amnesia.[10] Current discussion in the neuropsychiatry literature centers on whether PRA is possibly psychogenic or solely organic in nature.[10]


RA commonly results from damage to regions of the brain that are associated with episodic and declarative memory, including autobiographical information. In extreme cases, individuals may completely forget who they are. Generally, this is a more severe type of amnesia known as global, or generalized amnesia.[11] However, memory loss can also be selective or categorical, manifested by a person's inability to remember events related to a specific incident or topic. Patients also differ in durations of RA (how long they can't recall information) and durations of what is forgotten (past time frame for which information is unavailable).

During consolidation, the hippocampus acts as an intermediate tool that quickly stores new information until it is transferred to the neocortex for the long-term. The temporal lobe, which holds the hippocampus, entorhinal, perirhinal and parahippocampal cortices, has a reciprocal connection with the neocortex.[12] The temporal lobe is temporarily needed when consolidating new information; as the learning becomes stronger, the neocortex becomes more independent of the temporal lobe.[12]

Studies on specific cases demonstrate how particular impaired areas of the hippocampus are associated with the severity of RA. Damage can be limited to the CA1 field of the hippocampus, causing very limited RA for about one to two years.[12] More extensive damage limited to the hippocampus causes temporally graded amnesia for 15 to 25 years.[12] Another study suggests that large medial temporal lobe lesions, that extend laterally to include other regions, produce more extensive RA, covering 40 to 50 years.[12] These findings suggest that density of RA becomes more severe and long-term as the damage extends beyond the hippocampus to surrounding structures.

Traumatic brain injury (TBI)

Traumatic brain injury (TBI), also known as post-traumatic amnesia, occurs from an external force that causes structural damage to the brain, such as a sharp blow to the head, a diffuse axonal injury,[13] or childhood brain damage (e.g., shaken baby syndrome).[13] In cases of sudden rapid acceleration, the brain continues moving around in the skull, harming brain tissue as it hits internal protrusions.[14]

TBI varies according to impact of external forces, location of structural damage, and severity of damage ranging from mild to severe.[15][13][14] Retrograde amnesia can be one of the many consequences of brain injury but it is important to note that it is not always the outcome of TBI. An example of a subgroup of people who are often exposed to TBI are individuals who are involved in high-contact sports. Research on football players takes a closer look at some of the implications to their high-contact activities. Enduring consistent head injuries can have an effect on the neural consolidation of memory.[16]

Specific cases, such as that of patient ML, support the evidence that severe blows to the head can cause the onset of RA.[17] In this specific case there was an onset of isolated RA following a severe head injury. The brain damage did not affect the person's ability to form new memories. Therefore, the idea that specific sections of retrograde memory are independent of anterograde is supported. Normally, there is a very gradual recovery, however, a dense period of amnesia immediately preceding the trauma usually persists.[16]

Traumatic events

RA can occur without any anatomical damage to the brain, lacking an observable neurobiological basis.[18] Primarily referred to as psychogenic amnesia or psychogenic fugue, it often occurs due to a traumatic situation that individuals wish to consciously or unconsciously avoid through intrapsychic conflicts or unconscious repressions.[19] The onset of psychogenic amnesia can be either global (i.e., individual forgets all history) or situation specific (i.e., individual is unable to retrieve memories of specific situations).[20]

Patients experiencing psychogenic amnesia have impaired episodic memory, instances of wandering and traveling, and acceptance of a new identity as a result of inaccessible memories pertaining to their previous identity.[19]

Recent research has begun to investigate the effects of stress and fear-inducing situations with the onset of RA. Long-term potentiation (LTP) is the process by which there is a signal transmission between neurons after the activation of a neuron, which has been known to play a strong role in the hippocampus in learning and memory.[20] Common changes in the hippocampus have been found to be related to stress and induced LTP.[20] The commonalities support the idea that variations of stress can play a role in producing new memories as well as the onset of RA for other memories.[20] The amygdala plays a crucial role in memory and can be affected by emotional stimuli, evoking RA.[21]

Studies of specific cases, such as 'AMN', support evidence of traumatic experiences as a plausible cause of RA. AMN escaped a small fire in his house, did not inhale any smoke, and had no brain damage. Nevertheless, he was unable to recall autobiographical knowledge the next day. This case shows that RA can occur in the absence of structural brain damage.[22]

After a traumatic head injury, emotional disturbances can occur at three different levels: neurological, reactionary, and long-term disturbances. Neurological disturbances can change emotional and motivational responses. Reactionary disturbances effect emotional and motivational responses as well, but reflect the failure to cope with environmental demands. Someone with this might withdraw from the environment that they are placed in because they no longer know how to handle the cognitive resources.[23]

Nutritional deficiency

RA has been found among alcohol-dependent patients who have Korsakoff's syndrome.[24] Korsakoff's syndrome patients develop retrograde amnesia due to a thiamine deficiency (lack of vitamin B1).[25] Also, chronic alcohol use disorders are associated with a decrease in the volume of the left and right hippocampus.[24]

These patients' regular diet consists mostly of hard alcohol intake, which lacks the necessary nutrients for typical development and maintenance.[25] Therefore, after a prolonged time consuming primarily alcohol, these people undergo memory difficulties and ultimately develop RA. However, some of the drawbacks of using Korsakoff patients to study RA is the progressive nature of the illness and the unknown time of onset.[12]


Infections that pass the blood–brain barrier can cause brain damage (encephalitis), sometimes resulting in the onset of RA. In the case of patient 'SS', the infection led to focal or isolated retrograde amnesia where there was an absence of or limited AA. Brain scans show abnormalities in the bilateral medial temporal lobes, including two thirds of the hippocampal formation and the posterior part of the amygdala.[26]


Henry Molaison had epilepsy that progressed and worsened by his late twenties. The severity of his condition caused him to undergo surgery in an effort to prevent his seizures. Unfortunately, due to a lack of overall known neurological knowledge, Molaison's surgeons removed his bilateral medial temporal lobe, causing profound AA and RA.[27] The removed brain structures included the hippocampus, the amygdala, and the parahippocampal gyrus, now called the medial temporal lobe memory system.[27] HM was one of the most studied memory cases to date and started the examination of neurological structures in relation to memory.

Patients who have RA due to surgery are "P.B." and "F.C." who had unilateral removal of the medial areas in the left temporal lobe.[27]

Controlled induction

Clinically induced RA has been achieved using different forms of electrical induction.

Brain structures

The most commonly affected areas are associated with episodic and declarative memory such as the hippocampus,[32] the diencephalon,[33] and the temporal lobes.[34]

Brain plasticity has helped explain the recovery process of brain damage induced retrograde amnesia, where neuro-structures use different neural pathways to avoid the damaged areas while still performing their tasks.[39] Thus, the brain can learn to be independent of the impaired hippocampus, but only to a certain extent.[12] For example, older memories are consolidated over time and in various structures of the brain, including Wernicke's area and the neocortex, making retrieval through alternate pathways possible.[4]



As previously mentioned, RA can affect people's memories in different degrees, but testing is required to help determine if someone is experiencing RA. Several tests exist, for example, testing for factual knowledge such as known public events.[5] A problem with this form of testing is that people generally differ in their knowledge of such subjects.[5] The tests also have to be changed regularly to adapt to the period of time patients have been alive, and include questions about autobiographical events that range in amount of detail.[40] Due to the nature of the information being tested, it is often difficult to verify the accuracy of the memories being recalled, especially if they are from a distant past.[5] One way to confirm information is by consulting close family members or caregivers. Another problem that arises is that this type of testing can result in a significant amount of data that needs to be processed and confirmed.[40] Other ways to test someone is via autobiographical knowledge using the Autobiographical Memory Interview (AMI).[5] A test that comprises names of relatives, personal information, and job history. The AMI was created by Kopelman, Wilson, and Baddeley (1990). This information could help determine if someone is experiencing RA and the degree of memory affected. Some researchers have found that the time interval after the head injury occurred did not seem to matter. The effect of the memory loss was the same no matter how long it had been after from the injury.[41]

Brain abnormalities can be measured using magnetic resonance imaging (MRI), computed tomography scan (CT) and electroencephalography (EEG), which can provide detailed information about specific brain structures. In many cases, an autopsy helps identify the exact brain region affected and the extent of the damage that caused RA once the patient has died.

There are some aspects essential to the patient that remain unaffected by RA. In many patients, their personality remains the same.[42] Also, semantic memory, that is general knowledge about the world, is usually unaffected.[43] However, episodic memory, which refers to one's life experiences, is impaired.[44]

Another real life problem with RA is malingering, which is conceived as the rational output of a neurologically normal brain aiming at the surreptitious achievement of a well identified gain. Since it is common for people who have committed a crime to report having RA for that specific event in order to avoid their punishment, the legal system has pushed for the creation of a standardized test of amnesia. However, since most cases differ in onset, duration, and content forgotten, this task has shown to be a rather complex one.[45]

Spontaneous recovery

When someone has RA, their memory cannot be recovered by simply being informed about their personal experiences and their identity.[46] This is called reminder effect or reminder treatment. The reminder effect consists of re-exposing the patient to past personal information,[47] which cannot reverse RA.[48] Thus, reminding the patient about details of their life has no scientific bearings on recovering memory. Fortunately, memory can be and usually is recovered due to spontaneous recovery and plasticity.[46]

Case studies

Since researchers are interested in examining the effects of disrupted brain areas and conducting experiments for further understanding of an unaffected, normal brain,[49] many individuals with brain damage have volunteered to undergo countless tests to advance our scientific knowledge of the human brain. For example, Henry Molaison (HM) was someone with significant brain damage and participated in a lot of neurological research. Furthermore, he was also the most tested person in neuropsychology.[50] All living people who participate are referred to in literature using only their initials to protect privacy.

Each case of RA has led to different symptoms and durations, where some patients have exhibited an inability to describe future plans, whether in the near future (e.g., this afternoon) or in the distant future (e.g., next summer)[51] because of their inability to consolidate memories.[12] Furthermore, researchers have also found that some patients can identify themselves and loved ones in photographs, but cannot determine the time or place the photo was taken.[51] It has also been found that patients with RA greatly differ from the general population in remembering past events.[52]

A few case examples are:

Although it may seem that people living with brain damage have great difficulty continuing the usual day-to-day aspects, they still can accomplish many feats. People with RA are able to lead a normal life. For instance, KC is a man who has many functional aspects intact; normal intelligence, unaffected perceptual and linguistic skills, short-term memory, social skills, and reasoning abilities.[51] All of these things are necessary in everyday life and contribute to normal living. KC also is fully capable of scripted activities (e.g., making reservations or changing a flat tire).[51] In addition, patient HC successfully graduated high school and continued into post-secondary studies,[52] an obvious accomplishment despite her condition. DH relearned his childhood memories from his parents and can retell the stories, but cannot recall specifics other than what has been told to him.[1]

Other forms of amnesia

Other forms of amnesia exist and may be confused with RA. For instance, anterograde amnesia (AA) is the inability to learn new information.[54] This describes a problem encoding, storing, or retrieving information that can be used in the future.[55] It is important to note that these two conditions can, and often do both occur in the same patient simultaneously,[15] but are otherwise separate forms of amnesia.

RA can also be an inherent aspect of other forms of amnesia, namely transient global amnesia (TGA). TGA is the sudden onset of AA and RA caused by a traumatic event, however it is short lived, typically lasting only 4 to 8 hours[56] TGA is very difficult to study because of the patients' quick recovery.[57] This form of amnesia, like AA, remains distinct from RA.[12]

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.

Psychogenic amnesia, or dissociative amnesia, is a memory disorder characterized by sudden retrograde autobiographical memory loss, said to occur for a period of time ranging from hours to years.

See also


  1. ^ a b c Hunkin NM, Parkin AJ, Bradley VA, Burrows EH, Aldrich FK, Jansari A, Burdon-Cooper C (April 1995). "Focal retrograde amnesia following closed head injury: a case study and theoretical account". Neuropsychologia. 33 (4): 509–523. doi:10.1016/0028-3932(94)00136-D. PMID 7617158. S2CID 21295568.
  2. ^ Lafleche G, Verfaellie M (2017). "Anterograde Amnesia". In Kreutzer J, DeLuca J, Caplan B (eds.). Encyclopedia of Clinical Neuropsychology. Cham: Springer International Publishing. pp. 1–5. doi:10.1007/978-3-319-56782-2_1106-2. ISBN 978-3-319-56782-2.
  3. ^ a b c d e f g h i Lafleche G, Verfaellie M (2011). "Retrograde Amnesia". In Kreutzer J, DeLuca J, Caplan B (eds.). Encyclopedia of Clinical Neuropsychology. New York, NY: Springer New York. pp. 2167–2170. doi:10.1007/978-0-387-79948-3_1152. ISBN 978-0-387-79947-6.
  4. ^ a b c Wixted JT (February 2004). "The psychology and neuroscience of forgetting". Annual Review of Psychology. 55: 235–269. doi:10.1146/annurev.psych.55.090902.141555. PMID 14744216.
  5. ^ a b c d e Reed JM, Squire LR (May 1998). "Retrograde amnesia for facts and events: findings from four new cases". The Journal of Neuroscience : The Official Journal of the Society for Neuroscience. 18 (10): 3943–54. doi:10.1523/JNEUROSCI.18-10-03943.1998. PMC 6793126. PMID 9570821.
  6. ^ Bauer RM, Asken B (2008). "Chapter 28: The Three Amnesias". In Morgan JE, Ricker JH (eds.). Textbook of Clinical Neuropsychology (2nd ed.). New York, NY: Rutlidge. pp. 678–700. doi:10.4324/9781315537511-51. ISBN 978-1-351-98599-4.
  7. ^ Sehm B, Frisch S, Thöne-Otto A, Horstmann A, Villringer A, Obrig H (2011-10-19). de Beeck HP (ed.). "Focal retrograde amnesia: voxel-based morphometry findings in a case without MRI lesions". PLOS ONE. 6 (10): e26538. doi:10.1371/journal.pone.0026538. PMC 3197527. PMID 22028902.
  8. ^ a b c d Wheeler MA, McMillan CT (March 2001). "Focal retrograde amnesia and the episodic-semantic distinction". Cognitive, Affective & Behavioral Neuroscience. 1 (1): 22–36. doi:10.3758/CABN.1.1.22. PMID 12467101. S2CID 20269516.
  9. ^ a b c d e Miller LA, Caine D, Harding A, Thompson EJ, Large M, Watson JD (2001). "Right medial thalamic lesion causes isolated retrograde amnesia". Neuropsychologia. 39 (10): 1037–46. doi:10.1016/s0028-3932(01)00041-0. PMID 11440756. S2CID 18021762.
  10. ^ a b c d e f Lucchelli F, Muggia S, Spinnler H (1998). "The Syndrome of Pure Retrograde Amnesia". Cognitive Neuropsychiatry. 3 (2): 91–118. doi:10.1080/135468098396189.
  11. ^ Vaidya CJ, Gabrieli JD, Verfaellie M, Fleischman D, Askari N (April 1998). "Font-specific priming following global amnesia and occipital lobe damage". Neuropsychology. 12 (2): 183–92. doi:10.1037/0894-4105.12.2.183. PMID 9556765.
  12. ^ a b c d e f g h i Squire LR, Alvarez P (April 1995). "Retrograde amnesia and memory consolidation: a neurobiological perspective". Current Opinion in Neurobiology. 5 (2): 169–177. doi:10.1016/0959-4388(95)80023-9. PMID 7620304. S2CID 9080102.
  13. ^ a b c Wolf JA, Stys PK, Lusardi T, Meaney D, Smith DH (March 2001). "Traumatic axonal injury induces calcium influx modulated by tetrodotoxin-sensitive sodium channels". The Journal of Neuroscience : The Official Journal of the Society for Neuroscience. 21 (6): 1923–30. doi:10.1523/JNEUROSCI.21-06-01923.2001. PMC 6762603. PMID 11245677.
  14. ^ a b Hardman JM, Manoukian A (May 2002). "Pathology of head trauma". Neuroimaging Clinics of North America. 12 (2): 175–87, vii. doi:10.1016/s1052-5149(02)00009-6. PMID 12391630.
  15. ^ a b Winocur G, McDonald RM, Moscovitch M (2001). "Anterograde and retrograde amnesia in rats with large hippocampal lesions". Hippocampus. 11 (1): 18–26. doi:10.1002/1098-1063(2001)11:1<18::AID-HIPO1016>3.0.CO;2-5. PMID 11261769. S2CID 4079756.
  16. ^ a b Yarnell PR, Lynch S (April 1970). "Retrograde memory immediately after concussion". Lancet. 1 (7652): 863–864. doi:10.1016/S0140-6736(70)91691-0. PMID 4191508.
  17. ^ Levine B, Black SE, Cabeza R, Sinden M, Mcintosh AR, Toth JP, et al. (October 1998). "Episodic memory and the self in a case of isolated retrograde amnesia". Brain. 121 (Pt 10): 1951–1973. doi:10.1093/brain/121.10.1951. PMID 9798749.
  18. ^ Staniloiu A, Markowitsch HJ, Brand M (September 2010). "Psychogenic amnesia--a malady of the constricted self". Consciousness and Cognition. 19 (3): 778–801. doi:10.1016/j.concog.2010.06.024. PMID 20655759. S2CID 19950039.
  19. ^ a b Markowitsch HJ (November 2003). "Psychogenic amnesia". NeuroImage. 20 (Suppl 1): S132–S138. doi:10.1016/j.neuroimage.2003.09.010. PMID 14597306. S2CID 18671395.
  20. ^ a b c d Diamond DM, Park CR, Woodson JC (2004). "Stress generates emotional memories and retrograde amnesia by inducing an endogenous form of hippocampal LTP". Hippocampus. 14 (3): 281–91. doi:10.1002/hipo.10186. PMID 15132427. S2CID 45819426.
  21. ^ Strange BA, Hurlemann R, Dolan RJ (November 2003). "An emotion-induced retrograde amnesia in humans is amygdala- and beta-adrenergic-dependent". Proceedings of the National Academy of Sciences of the United States of America. 100 (23): 13626–13631. doi:10.1073/pnas.1635116100. PMID 14595032.
  22. ^ Markowitsch HJ, Kessler J, Van Der Ven C, Weber-Luxenburger G, Albers M, Heiss WD (January 1998). "Psychic trauma causing grossly reduced brain metabolism and cognitive deterioration". Neuropsychologia. 36 (1): 77–82. doi:10.1016/s0028-3932(97)00093-6. PMID 9533390. S2CID 19174159.
  23. ^ Prigatano GP (1987). "Psychiatric aspects of head injury: Problem areas and suggested guidelines for research". Neurobehavioral Recovery from Head Injury. New York: Oxford University Press. pp. 217–218.
  24. ^ a b De Bellis MD, Clark DB, Beers SR, Soloff PH, Boring AM, Hall J, Kersh A, Keshavan MS (May 2000). "Hippocampal volume in adolescent-onset alcohol use disorders". The American Journal of Psychiatry. 157 (5): 737–44. doi:10.1176/appi.ajp.157.5.737. PMID 10784466. S2CID 1668456.
  25. ^ a b McEntee WJ, Mair RG (August 1990). "The Korsakoff syndrome: a neurochemical perspective". Trends in Neurosciences. 13 (8): 340–4. doi:10.1016/0166-2236(90)90146-2. PMID 1699320. S2CID 31404753.
  26. ^ Fujii T, Yamadori A, Endo K, Suzuki K, Fukatsu R (December 1999). "Disproportionate retrograde amnesia in a patient with herpes simplex encephalitis". Cortex; A Journal Devoted to the Study of the Nervous System and Behavior. 35 (5): 599–614. doi:10.1016/S0010-9452(08)70822-0. PMID 10656630. S2CID 4480119.
  27. ^ a b c Squire LR (January 2009). "The legacy of patient H.M. for neuroscience". Neuron. 61 (1): 6–9. doi:10.1016/j.neuron.2008.12.023. PMID 19146808. S2CID 643599.
  28. ^ Ottosson J (1960). "Experimental studies of the mode of action of electroconvulsive therapy". Acta Psychiatrica Scandinavica. 145: 1–41. doi:10.1111/j.1600-0447.1960.tb08352.x. S2CID 29773758.
  29. ^ Donahue AB (June 2000). "Electroconvulsive therapy and memory loss: a personal journey". The Journal of ECT. 16 (2): 133–43. doi:10.1097/00124509-200006000-00005. PMID 10868323. S2CID 28318459.
  30. ^ Squire LR (1986). "Memory functions as affected by electroconvulsive therapy". Annals of the New York Academy of Sciences. 462: 307–314. doi:10.1111/j.1749-6632.1986.tb51265.x. PMID 3458411. S2CID 28060335.
  31. ^ Rao SK, Andrade C, Reddy K, Madappa KN, Thyagarajan S, Chandra S (May 2002). "Memory protective effect of indomethacin against electroconvulsive shock-induced retrograde amnesia in rats". Biological Psychiatry. 51 (9): 770–773. doi:10.1016/S0006-3223(01)01219-7. PMID 11983192. S2CID 29560202.
  32. ^ a b Cipolotti L, Shallice T, Chan D, Fox N, Scahill R, Harrison G, Stevens J, Rudge P (2001). "Long-term retrograde amnesia...the crucial role of the hippocampus". Neuropsychologia. 39 (2): 151–72. doi:10.1016/s0028-3932(00)00103-2. PMID 11163373. S2CID 7428309.
  33. ^ a b Dusoir H, Kapur N, Byrnes DP, McKinstry S, Hoare RD (December 1990). "The role of diencephalic pathology in human memory disorder. Evidence from a penetrating paranasal brain injury". Brain. 113 (Pt 6): 1695–1706. doi:10.1093/brain/113.6.1695. PMID 2276041.
  34. ^ a b Buccione I, Fadda L, Serra L, Caltagirone C, Carlesimo GA (November 2008). "Retrograde episodic and semantic memory impairment correlates with side of temporal lobe damage". Journal of the International Neuropsychological Society : JINS. 14 (6): 1083–94. doi:10.1017/S1355617708080922. PMID 18954490. S2CID 12905302.
  35. ^ Nadel L, Moscovitch M (April 1997). "Memory consolidation, retrograde amnesia and the hippocampal complex". Current Opinion in Neurobiology. 7 (2): 217–227. doi:10.1016/S0959-4388(97)80010-4. PMID 9142752. S2CID 4802179.
  36. ^ Reinvang I, Nielsen CS, Gjerstad L, Bakke SJ (September 2000). "Isolated retrograde amnesia: Evidence for preservation of implicit memory. An event-related potential investigation". Neurocase. 6 (5): 423–433. doi:10.1080/13554790008402713. S2CID 145665210.
  37. ^ Milner B (1968). "Visual recognition and recall after right temporal lobe excision in man". Neuropsychologia. 6 (3): 191–209. doi:10.1016/0028-3932(68)90019-5.
  38. ^ Kolb B, Whishaw I (1990). Fundamentals of Human Neuropsychology (3rd ed.). New York: Freeman. ISBN 978-0-7167-1973-1.[page needed]
  39. ^ Kolb B, Gibb R, Robinson TE (February 2003). "Brain plasticity and behavior". Current Directions in Psychological Science. 12 (1): 1–5. doi:10.1111/1467-8721.01210. hdl:2027.42/74427. S2CID 11271886.
  40. ^ a b Baddeley A, Eysenck MW, Anderson MC (2015). Memory. New York: Psychology Press. pp. 444–48.
  41. ^ Crovitz HF, Daniel WF (December 1987). "Length of retrograde amnesia after head injury: a revised formula". Cortex; A Journal Devoted to the Study of the Nervous System and Behavior. 23 (4): 695–8. doi:10.1016/s0010-9452(87)80060-6. PMID 3443004. S2CID 4480557.
  42. ^ Scoville WB, Milner B (February 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.
  43. ^ Markowitsch HJ, Calabrese P, Liess J, Haupts M, Durwen HF, Gehlen W (September 1993). "Retrograde amnesia after traumatic injury of the fronto-temporal cortex". Journal of Neurology, Neurosurgery, and Psychiatry. 56 (9): 988–92. doi:10.1136/jnnp.56.9.988. PMC 489734. PMID 8410040.
  44. ^ Tulving E, Markowitsch HJ (1998). "Episodic and declarative memory: role of the hippocampus". Hippocampus. 8 (3): 198–204. doi:10.1002/(SICI)1098-1063(1998)8:3<198::AID-HIPO2>3.0.CO;2-G. PMID 9662134. S2CID 18634842.
  45. ^ Wiggins EC, Brandt J (March 1988). "The detection of simulated amnesia". Law and Human Behavior. 12 (1): 57–78. doi:10.1007/BF01064274. S2CID 144312526.
  46. ^ a b Cherkin A (May 1972). "Retrograde amnesia in the chick: Resistance to the reminder effect". Physiology & Behavior. 8 (5): 949–955. doi:10.1016/0031-9384(72)90309-5.
  47. ^ Millin PM, Moody EW, Riccio DC (January 2001). "Interpretations of retrograde amnesia: old problems redux". Nature Reviews. Neuroscience. 2 (1): 68–70. doi:10.1038/35049075. PMID 11253361. S2CID 205012306.
  48. ^ de Hoz L, Martin SJ, Morris RG (August 2004). "Forgetting, reminding, and remembering: the retrieval of lost spatial memory". PLOS Biology. 2 (8): E225. doi:10.1371/journal.pbio.0020225. PMC 509297. PMID 15314651.
  49. ^ Esclapez M, Tillakaratne NJ, Kaufman DL, Tobin AJ, Houser CR (March 1994). "Comparative localization of two forms of glutamic acid decarboxylase and their mRNAs in rat brain supports the concept of functional differences between the forms". The Journal of Neuroscience : The Official Journal of the Society for Neuroscience. 14 (3 Pt 2): 1834–1855. doi:10.1523/JNEUROSCI.14-03-01834.1994. PMC 6577546. PMID 8126575.
  50. ^ Corkin S, Amaral DG, González RG, Johnson KA, Hyman BT (May 1997). "H. M.'s medial temporal lobe lesion: findings from magnetic resonance imaging". The Journal of Neuroscience : The Official Journal of the Society for Neuroscience. 17 (10): 3964–79. doi:10.1523/JNEUROSCI.17-10-03964.1997. PMC 6573687. PMID 9133414.
  51. ^ a b c d Tulving E, Schacter DL, McLachlan DR, Moscovitch M (August 1988). "Priming of semantic autobiographical knowledge: a case study of retrograde amnesia". Brain and Cognition. 8 (1): 3–20. doi:10.1016/0278-2626(88)90035-8. PMID 3166816. S2CID 17125951.
  52. ^ a b Kwan D, Carson N, Addis DR, Rosenbaum RS (September 2010). "Deficits in past remembering extend to future imagining in a case of developmental amnesia". Neuropsychologia. 48 (11): 3179–3186. doi:10.1016/j.neuropsychologia.2010.06.011. PMID 20561535. S2CID 565582.
  53. ^ a b c d e f Fujiwara E, Brand M, Kracht L, Kessler J, Diebel A, Netz J, Markowitsch HJ (January 2008). "Functional retrograde amnesia: a multiple case study". Cortex; A Journal Devoted to the Study of the Nervous System and Behavior. 44 (1): 29–45. doi:10.1016/j.cortex.2005.09.001. PMID 18387529. S2CID 206982684.
  54. ^ Dworetzky BA (2001). "The neurology of memory". Seminars in Speech and Language. 22 (2): 95–105. doi:10.1055/s-2001-13934. PMID 11373070.
  55. ^ Markowitsch HJ, Calabrese P (1999). "Neuroanatomy of memory". In Tulving E, Craik FI (eds.). The Oxford Handbook of Memory. Oxford University Press. pp. 465–484.
  56. ^ Fisher CM (October 1982). "Transient global amnesia. Precipitating activities and other observations". Archives of Neurology. 39 (10): 605–8. doi:10.1001/archneur.1982.00510220003001. PMID 7125972.
  57. ^ Guillery-Girard B, Desgranges B, Urban C, Piolino P, de la Sayette V, Eustache F (November 2004). "The dynamic time course of memory recovery in transient global amnesia". Journal of Neurology, Neurosurgery, and Psychiatry. 75 (11): 1532–1540. doi:10.1136/jnnp.2003.024968. PMID 15489382. S2CID 16685800.
  58. ^ Woodruff B, Patria M (19 April 2010). "Man With Amnesia Lost 46 Years in Workplace Slip: Scott Bolzan Interviews Wife for Details on Their 25-Plus Year Marriage, Past Life". Nightline. ABC News.