Retrograde amnesia

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Retrograde amnesia
Classification and external resources
ICD-10 R41.2
ICD-9-CM 780.9

Retrograde amnesia (RA) is a loss of memory-access to events that occurred, or information that was learned, before an injury or the onset of a disease.[1] It tends to negatively affect episodic, autobiographical, and declarative memory while usually keeping procedural memory intact with no difficulty for learning new knowledge. RA can be temporally graded or more permanent based on the severity of its cause and is usually consistent with Ribot's Law: where subjects are more likely to lose memories closer to the traumatic incident than more remote memories.[2] The type of information that is forgotten can be very specific, like a single event, or more general, resembling generic amnesia. It is not to be confused with anterograde amnesia, which deals with the inability to form new memories following the onset of an injury or disease.


Brain structures[edit]

The most commonly affected areas are associated with episodic and declarative memory such as the hippocampus,[3] the diencephalon,[4] and the temporal lobes.[5]

  • The hippocampus deals largely with memory consolidation,[3] where information from the working memory and short-term memory is encoded into long-term storage for future retrieval. Amnesic patients with damage to the hippocampus are able to demonstrate some degree of unimpaired semantic memory, despite a loss of episodic memory, due to spared parahippocampal cortex.[6] In other words, retrograde amnesics "know" an information or skill, but cannot "remember" how they do.
  • The diencephalon and the surrounding areas' role in memory is not well understood. However, this structure appears to be involved in episodic memory recall.[4]
  • The temporal lobes are essential for semantic and factual memory processing. Aside from helping to consolidate memory with the hippocampus,[5] the temporal lobes are extremely important for semantic memory. Damage to this region of the brain can result in the impaired organization and categorization of verbal material, disturbance of language comprehension, and impaired long-term memory. The right frontal lobe is critical for the retrieval of episodic information, while the left frontal region is more active for the retrieval of semantic information. [56] Lesions in the right hemisphere and right frontal lobes result in the impaired recall of non-verbal material, such as music and drawings.[7] Difficulties in studying this region of the brain extends to its duties in comprehension, naming objects, verbal memory, and other language functions.[8]

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.[9] Thus, the brain can learn to be independent of the impaired hippocampus, but only to a certain extent.[10] 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.[2]

Types of retrograde amnesia[edit]

As previously mentioned, RA commonly results from damage to the brain regions most closely 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 differs 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).

Temporally graded retrograde amnesia[edit]

In temporally graded retrograde amnesia, victims eventually recover most memories following the onset of RA. This suggests that the hippocampal formation is only used in systematic consolidation for temporary, and short periods of times, until long-term consolidation takes place in other brain structures.[12] Here, the fact that damage to the hippocampal formation can eventually overcome RA suggests that other brain structures are able to take over the jobs of the malfunctioning regions. RA can also progress and further deteriorate memory recollection, as in the case of Korsakoff syndrome and Alzheimer's disease, due to the ongoing nature of the damage caused by the illnesses. The degree to which different patients recover from RA differs in time (some take a few days while others a few decades) and content (some will only remember certain specific instances while others more).

Focal, isolated, and pure retrograde amnesia[edit]

These terms are used to describe a pure form of RA, with an absence of anterograde amnesia (AA). In addition, Focal RA in particular, has also been used to describe a RA situation in which there is a lack of observable physical deficit as well.[13] This could be described as a psychogenic form of amnesia with mild anterograde and retrograde loss.[1] A case study of DH revealed that the patient was unable to provide personal or public information, however there was no parahippocampal or entorhinal damage found.[1] Individuals with focal brain damage have minimal RA.[14]

Isolated RA is associated with a visible thalamic lesion.[15] Consistent with other forms of RA, the isolated form is marked by a profound inability to recall past information.[15]

Pure retrograde amnesia (PRA) refers to the behavioral syndrome that is characterized by the inability to retrieve remote information in the face of a normal ability to learn new information, with no other ecological or psychometric evidence of cognitive impairment. It should not be confused with the brief periods of peritraumatic amnesia that are common in mild concussive head traumas. The findings of pure retrograde amnesia have helped form the dissociation between mechanisms for RA and AA. Several studies have found numerous causes for PRA like vascular diseases, head traumas ranging from mild to severe, encephalitis, as well as purely psychological conditions and totally unidentifiable aetiologies. Most people who suffer from PRA can function normally and learn new information and therefore are not severely set back in life. [57] (Lucchelli, Muggia, & Spinnler, 1998).

A pure form of RA is rare as most cases of RA co-occur with AA. A famous example is that of patient ML. The patient's MRI revealed damage to the right ventral frontal cortex and underlying white matter, including the uncinate fasciculus, a band of fibres previously thought to mediate retrieval of specific events from one's personal past.[16]

Causes[edit]

The causal explanation of retrograde amnesia is still under investigation.

The three main models used to explain RA assume that the hippocampus is one of the main areas of the brain used in memory consolidation.[6] 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.[10] The temporal lobe is temporarily needed when consolidating new information; as the learning becomes stronger, the neocortex becomes more independent of the temporal lobe.[10]

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 1 to 2 years.[10] More extensive damage limited to the hippocampus causes temporally graded amnesia for 15 to 25 years.[10] Another study also suggested that large medial temporal lobe lesions, that extends laterally to include other regions, produces more extensive RA, covering 40 to 50 years.[10] These findings suggest that density of RA becomes more severe and long-term as the damage extends beyond the hippocampus to surrounding structures.

The common studied causes of RA do not always lead to the onset of RA. It may even be that in some cases both conscious feigning and unconscious processes are at play. [56]

Traumatic brain injury (TBI) or post-traumatic amnesia[edit]

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,[17] or childhood brain damage (e.g., shaken baby syndrome).[17] In cases of sudden rapid acceleration, the brain continues moving around in the skull, harming brain tissue as it hits internal protrusions.[18]

TBI varies according to impact of external forces, location of structural damage, and severity of damage ranging from mild to severe.[12][17][18] 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.[19]

Specific cases, such as that of patient ML, support the evidence that severe blows to the head can cause the onset of RA.[16] 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.[19]

Traumatic events[edit]

RA can occur without any anatomical damage to the brain, lacking an observable neurobiological basis.[20] 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.[21][57] 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).[22]

People 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.[21]

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.[22] Common changes in the hippocampus have been found to be related to stress and induced LTP.[22] 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.[22] Also, the amygdala plays a crucial role in memory and can be affected by emotional stimuli, evoking RA.[23]

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. Surprisingly, the next day, he was unable to recall autobiographical based knowledge. This case shows that RA can occur in the absence of structural brain damage.[24]

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 they reflect 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.[25]

Nutritional deficiency[edit]

RA has been found among alcohol-dependent patients who suffer from Korsakoff syndrome.[26] Korsakoff syndrome patients suffer from retrograde amnesia due to a thiamine deficiency (lack of vitamin B1).[27] Also, chronic alcohol use disorders are associated with a decrease in volume of the left and right hippocampus.[26]

These patients' regular diet consists mostly of hard alcohol intake, which lacks the necessary nutrients for healthy development and maintenance.[27] Therefore, after a prolonged time consuming primarily alcohol, these people undergo memory difficulties and ultimately suffer from RA. However, some of the drawback of using Korsakoff patients to study RA is the progressive nature of the illness and the unknown time of onset.[10]

Infections[edit]

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.[28]

Surgery[edit]

Henry Molaison suffered from 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.[29] The removed brain structures included the hippocampus, the amygdala, and the parahippocampal gyrus, now called the medial temporal lobe memory system.[29] HM was one of the most studied memory cases to date and started the examination of neurological structures in relation to memory.

Other patients who suffered RA due to surgery are 'P.B.' and 'F.C.' who had unilateral removal of the medial areas in the left temporal lobe.[29]

Controlled induction[edit]

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

  • Electroconvulsive therapy (ECT), used as a depression therapy, can cause impairments in memory.[30] Tests show that information of days and weeks before the ECT can be permanently lost.[31] The results of this study also show that severity of RA is more extreme in cases of bilateral ECT rather than unilateral ECT. Impairments can also be more intense if ECT is administered repetitively (sine wave simulation) as opposed to a single pulse (brief-pulse stimulation).[32]
  • Electroconvulsive shock (ECS): The research in this field has been advanced by using animals as subjects.[33] Researchers induce RA in rats, for example, by giving daily ECS treatments.[34] This is done to further understand RA.

Diagnosis and treatment[edit]

Testing for retrograde amnesia[edit]

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.[35] A problem with this form of testing is that people generally differ in their knowledge of such subjects.[35] Other ways to test someone is via autobiographical knowledge using the Autobiographical Memory Interview (AMI),[35] comprising names of relatives, personal information, and job history. This information could help determine if someone is experiencing RA and the degree of memory affected. However, 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.[35] 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.[36]

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.[37] Also, semantic memory, that is general knowledge about the world, is usually unaffected.[38] However, episodic memory, which refers to one's life experiences, is impaired.[39]

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. [56] 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.[40]

Spontaneous recovery[edit]

When someone is suffering from RA, their memory cannot be recovered from simply being told personal experiences and their identity.[41] This is called reminder effect or reminder treatment. The reminder effect consists of re-exposing the patient to past personal information,[42] which cannot reverse RA.[43] Thus, reminding the patient 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.[41]

Case studies[edit]

Since researchers are interested in examining the effects of disrupted brain areas and conducting experiments for further understanding of an unaffected, normal brain,[44] 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.[45] 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)[46] because of their inability to consolidate memories.[10] 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.[46] It has also been found that patients with RA greatly differ from the general population in remembering past events.[47]

A few case examples are:

  • After a head injury, AB had to relearn personal information.[48] Many of AB’s habits had also changed.[48]
  • Patient CD, reported disorientation of place and time following his injuries as well as relearning previously learned information and activities (e.g., using a razor).[48]
  • EF was examined and found to be very confused about social norms (e.g., appropriate attire outside his home). EF exhibited memory loss of his personal experiences (e.g., childhood), and the impaired ability to recognize his wife and parents.[48]
  • JG is the first recorded patient suffering from isolated RA.[15]
  • GH, a mother and a wife, had surgery in August 2002. When GH woke up after the surgery, she believed it was May 1989.[48] Due to her amnesia, GH experienced great difficulty in her social environment, being overwhelmed by relationships to others.[48]
  • DH, a learning disabilities instructor and husband, suffered a closed head injury. He did not show any normal signs of memory loss but he could not recall anything prior to the accident.[1]
  • CDA is 20-year-old man who fell and experienced head trauma after being unconscious for a little less than an hour. He had a self-identity loss and a retrograde deficit limited to the autobiographical events 5 years before the trauma. He often showed signs of spontaneous speech that was iterative and sometimes incoherent. When he saw his family and friends, he was shocked at how old they looked because he remembered them from 5 years earlier. This case also included amnesia for procedural skills like the fear of shaving or driving, which ultimately was overcome. There were no psychological, neuropsychological, or brain damage problems. His recovery of memory was progressive and spontaneous, where after several months the amnesia was limited to the two years preceding the trauma. This was a classic case of PRA. [57]
  • GC was a 38 year old accountant that was found in a town square unable to remember anything about himself and unaware of where he was and how he got there. He was eventually able to recall basic information about himself and his family, but could not recall emotionally charged autobiographical events pertaining to the last 7 years of his life. Within 3–4 days, it was determined that his autobiographical amnesia was clearly and strictly selective for professional events, as he could remember everything that was not related to his job. It was ultimately learned that the job had created severe emotional stress and anxiety due to the extreme hours that triggered a sudden fugue state. He was eventually able to recover most of his memories minus a single work event where he had stolen money from the company. This was a classic case of psychogenic amnesia. [57]
  • AF is a 15-year-old boy who hit his head and lost consciousness. He could not remember anything but was able to play songs on the piano, showing that his procedural memory was still intact. He gradually recovered some memories within the first 2–3 days but had autobiographical amnesia as well as significant memory loss for famous public facts and events for the 2 years prior to the injury. [57]

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.[46] 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).[46] In addition, patient HC successfully graduated high school and continued into post-secondary studies,[47] 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[edit]

Other forms of amnesia exist and may be confused with RA. For instance, anterograde amnesia (AA) is the inability to learn new information.[49] This describes a problem encoding, storing, or retrieving information that can be used in the future.[50] It is important to note that these two conditions can, and often do both occur in the same patient simultaneously,[12] 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.[51] TGA is very difficult to study because of the patients' quick recovery.[52] This form of amnesia, like AA, remains distinct from RA.[10]

Post-traumatic amnesia (PTA) is a state of confusion that occurs immediately following a traumatic brain injury in which the injured person isdisoriented 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[edit]

References[edit]

  1. ^ a b c d e Hunkin, N., Parkin, A., Bradley, V., Burrows, E., Aldrich, F., Jansari, A., & Burdon-Cooper, C. (1995) Focal retro grade amnesia following closed head injury: A case study and theoretical account, Neuropsychologia, 33(4) 509-523. doi:10.1016/0028-3932(94)00136-D
  2. ^ a b Wixted, J. T. (2004). The psychology and neuroscience of forgetting, Annual Review of Psychology, 55, 235-269. doi:10.1146/annurev.psych.55.090902.141555
  3. ^ 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), 151–172.
  4. ^ a b Dusoir, H., Kapur, N., Byrnes, D. P., McKinstry, S., & Hoare, S. D. (1990). The role of diencephalic pathology in human memory disorder: Evidence from a penetrating paranasal brain injury, Brain, 113(6), 1695-1706. doi:10.1093/brain/113.6.1695
  5. ^ a b Buccione, I., Fadda, L., Serra, L., Caltagirone, C., & Carlesimo, G. (2008). Retrograde episodic and semantic memory impairment correlates with side of temporal lobe damage, Journal of the International Neuropsychological Society, 14(6), 1083-1094.
  6. ^ a b Nadel, L., & Moscovitch, M. (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
  7. ^ Milner, B. (1968). Visual recognition and recall after right temporal lobe excision in man, Neuropsychologia, 6, 191-209.
  8. ^ Kolb, B., & Whishaw, I. (1990). Fundamentals of human neuropsychology. W.H. Freeman and Co., New York.
  9. ^ Kolb, B., & Gibb, R. (2003). Brain plasticity and behavior, Current Directions in Psychological Science, 12(1), 1-5. doi:10.1111/1467-8721.01210
  10. ^ a b c d e f g h i Squire, L. R., & Alvarez, P. (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
  11. ^ Vaidya, C. J., Gabrieli, J. D. E., Mieke, F. D., & Askari, N. (1998). Font-specific priming following global amnesia and occipital lobe damage, Neuropsychology, 12(2), 183-192.
  12. ^ a b c Winocur, G., McDonald, R. M., & Moscovitch, M. (2001). Anterograde and retrograde amnesia in rats with large hippocampal lesions, Hippocampus, 11, 18-26.
  13. ^ Evans, J. J., Breen, E. K., Antoun, N., & Hodges, J. R. (1996). Focal retrograde amnesia for autobiographical events following cerebral vasculitis: A connectionist account, Neurocase, 2(1), 1-11.
  14. ^ Kapur, N., Ellison, D., Smith, M. P., McLellan, D. L., & Burrows, E. H. (1992). Focal retrograde amnesia following bilateral temporal lobe pathology, Brain, 115(1), 73-85. doi:10.1093/brain/115.1.73
  15. ^ a b c Miller, L. A., Caine, D., Harding, A., Thompson, E. J., Large, M., & Watson, J. D. G. (2001). Right medial thalamic lesion causes isolated retrograde amnesia, Neuropsychologia, 39, 1037-1046.
  16. ^ a b Levine, B., Black, S. E., Cabeza, R., Sinden, M., Mcintosh, A. R., Toth, J. P., Tulving, E., & Stuss, D. T. (1998). Episodic memory and the self in a case of isolated retrograde amnesia, Brain, 121(10), 1951-1973. doi:10.1093/brain/121.10.1951
  17. ^ a b c Wolf, J.A., Stys, P. K., Lusardi, T., Meaney, D., & Smith, D. H. (2001). Traumatic axonal injury induces calcium influx modulated by tetrodotoxin-sensitive sodium channels, Journal of Neuroscience, 21(6), 1923–1930
  18. ^ a b Hardman, J. M., & Manoukian, A. (2002). Pathology of head trauma, Neuroimaging Clinics of North America, 12(2), 175–187
  19. ^ a b Yarnell, P. R., & Lynch, S. (2007). Retrograde memory immediately after a concussion, The Lancet, 295(7652), 863-864. doi:10.1016/S0140-6736(70)91691-0
  20. ^ Stanilou, A., Markowitsch, H. J., & Brand, M. (2010). Psychogenic amnesia – A malady of the constricted self, Consciousness and Cognition: An International Journal, 19(3), 778-801.
  21. ^ a b Markowitsch, H. J. (2003). Psychogenic amnesia, NeuroImage, 20(1), S132-S138. doi:10.1016/j.neuroimage.2003.09.010
  22. ^ a b c d Diamond, D. M., Park, C. R., & Woodson, J. C. (2004). Stress generates emotional memories and retrograde amnesia by inducing an endogenous form of hippocampal LTP, Hippocampus, 14(3), 281-291.
  23. ^ Strange, B. A., Hurlemann, R., & Dolan, J. R. (2003). An emotion-induced retrograde amnesia in humans is amygdala- and β-adrenergic-dependent, PNAD, 100(23), 13626-13631. doi:10.1073/pnas.1635116100
  24. ^ Markowitsch, H. J., Kessler, J., Van Der Ven, C., Weber-Luxenburger, G., Albers, M., & Heiss, W-D. (1998). Psychic trauma causing grossly reduced brain metabolism and cognitive deterioration, Psychologia, 36(1), 77-82.
  25. ^ Prigatano, G. (1987). Psychiatric aspects of head injury: Problem areas and suggested guidelines for research. Neurobehavioral Recovery from Head Injury, 217-218. New York: Oxford University Press.
  26. ^ a b De Bellis, M. D., Clark, D. B., Beers, S. R., Soloff, P. H., Boring, A. M., Hall, J., Kersh, A., & Keshavan, M. S. (2000). Hippocampal volume in adolescent-onset alcohol use disorder, The American Journal of Psychiatry, 157, 737-744.
  27. ^ a b McEntee, W. J., & Mair, R. G. (1990). The Korsakoff syndrome: A neurochemical perspective, Trends in Neurosciences, 13(8), 340-344.
  28. ^ Fujii, T., Yamadori, A., Endo, K., Suzuki, K., & Fukatsu, R. (1999). Disproportionate retrograde amnesia in a patient with herpes simplex encephalitis, Cortex 35(5), 599-614. doi:10.1016/S0010-9452(08)70822-0
  29. ^ a b c Squire, L. R. (2009). The legacy of patient H.M. for neuroscience, Neuron, 61, 6-10. doi:10.1016/j.neuron.2008.12.023
  30. ^ Ottosson, J-O. (1960). Experimental studies of memory impairment after electroconvulsive therapy, Acta Psychiatrica Scandinavica, 35(S145), 103-131. doi:10.1111/j.1600-0447.1960.tb08352.x
  31. ^ Donahue, A. B. (2000). Electroconvulsive therapy and memory loss: A personal journey, Journal of ECT, 16(2), 133-143.
  32. ^ Squire, L. R. (1986). Memory functions as affected by electroconvulsive therapy, Annals of the New York Academy of Science, 462, 307-314. doi:10.1111/j.1749-6632.1986.tb51265.x
  33. ^ Misanin, J. R., Miller, R. R., & Lewis, D. J. (1986). Retrograde amnesia produced by electroconvulsive shock after reactivation of consolidated memory trace, Science, 160(3827), 554-555.
  34. ^ Rao, S. K., Andrade, C., Reddy, K., Madappa, K. N., Thyagarajan, S., & Chandra, S. (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
  35. ^ a b c d Reed, J. M., & Squire, L. R. (1998). Retrograde amnesia for facts and events: Findings from four new cases, The Journal of Neuroscience, 18(10), 3943-3954.
  36. ^ Crovitz, H. & Daniel, W. (1987) Length of retrograde amnesia after head injury: A revised formula, Cortex, 23(4) 695-698 doi:10.1016/S0010-9452(87)80060-6
  37. ^ Scoville, W. B., & Milner, B. (2000). Loss of recent memory after bilateral hippocampal regions, Journal of Neuropsychiatry & Clinical Neurosciences, 12, 103-113.
  38. ^ Markowitsch, H. J., Calabrese, P., Liess, J., Haupts, M., Durwen, H. F., & Gehlen, W. (1993). An individual may be able to complete learned tasks but have no recollection of having learned them. Retrograde amnesia after traumatic injury of the fronto-temporal cortex, Journal of Neurology, Neurosurgery, and Psychiatry, 56, 988-992.
  39. ^ Tulving, E., & Markowitsch, H. J. (1998). Episodic and declarative memory: Role of the hippocampus, Hippocampus, 8, 198-204.
  40. ^ Wiggins, E. C., & Brandt, J. (1988). The detection of simulated amnesia, Law and Human Behavior, 12(1), 57-78. doi:10.1007/BF01064274
  41. ^ a b Cherkin, A. (1972). Retrograde amnesia in the chick: Resistance to the reminder effect, Physiology and Behavior, 8, 949-955.
  42. ^ Millin, P. M., Moody, E. W., & Riccio, D. C. (2001). Interpretations of retrograde amnesia: Old problems redux, Nature Reviews Neuroscience, 2, 68-70. doi:10.1038/35049075
  43. ^ de Hoz, L., Martin, S. J., & Morris, R. G. M. (2004). Forgetting, reminding, and remembering: The retrieval of lost spatial memory, PLOS Biology, 2(8), 225-235.
  44. ^ Esclapez, M., Tillakaratne, N. J., Kaufman, D. L., Tobin, A. J., & Houser, C. R. (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, 14(3), 1834-1855
  45. ^ Corkin, S., Amaral, D. G., Gonzalez, R. G., Johnson, K. A., & Hyman, B. T. (1997). H. M.’s medial temporal lobe lesion: Findings from magnetic resonance imaging, The Journal of Neuroscience, 17(10), 3964-3979.
  46. ^ a b c d Tulving, E., Schacter, D. L., McLachlan, D. R., & Moscovitch, M. (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
  47. ^ a b Kwan, D., Carson, N., Addis, D. R., & Rosenbaum, R. S. (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
  48. ^ a b c d e f Fujiwara, E., Brand, M., Kratcht, L., Kessler, J., Diebel, A., Netz, J., & Markowtsch, H. J. (2008). Functional retrograde amnesia: A multiple case study, Cortex, 44, 29-45. doi:10.1016/j.cortex.2005.09.001
  49. ^ Dworetzky, B. A. (2001). The neurology of memory, Seminars in Speech and Language, 22(2), 97-108. doi:10.1055/s-2001-13934
  50. ^ Markowitsch, H. J., & Calabrese, P. (1999). Neuroanatomy of memory. In The Oxford Handbook of Memory (Tulving, E., & Craik, F.I.M., eds), pp. 465–484, Oxford University Press.
  51. ^ Fisher, C. M. (1982). Transient global amnesia, Archives of Neurology, 39(10), 605-608.
  52. ^ Guillery-Girard, B., Desgranges, B., Urban, C., Piolino, P., de la Sayette, V., & Eustache, F. (2004). The dynamic time course of memory recovery in transient global amnesia, Journal of Neurology, Neurosurgery, and Psychiatry, 75, 1532-1540. doi:10.1136/jnnp.2003.024968
  53. ^ "Man With Amnesia Lost 46 Years in Workplace Slip: Scott Bolzan Interviews Wife for Details on Their 25-Plus Year Marriage, Past Life" by Bob Woodruff and Melia Patria, ABC News, "Nightline," April 19, 2010 http://abcnews.go.com/Nightline/amnesia-man-hits-head-loses-memories/story?id=10396719
  54. ^ "Couple behind 'The Vow': Kim and Krickitt Carpenter coming to Chattanooga" by Susan Pierce, "Chattanooga Times Free Press," September 17, 2013 http://www.timesfreepress.com/news/life/entertainment/story/2013/sep/17/the-couple-behind-the-vow/118725/

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